BUSINESS

Overview

GeoVax Labs, Inc. was formed in 2001 and(“GeoVax” or the “Company”) is a clinical-stage biotechnology company developing human vaccines thatagainst infectious diseases using our novel vaccine platform. Our platform supports production of non-infectious virus-like particles (VLPs) from the cells of the person receiving the vaccine. Producing non-infectious virus-like particles in the person being vaccinated circumvents the need to purify virus-like particles for inoculation. The production of virus-like particles in the person being vaccinated mimics a natural infection, stimulating both the humoral and cellular arms of the immune system to recognize, prevent and control human immunodeficiency virus (HIV). HIV infections result in acquired immunodeficiency syndrome (AIDS). We are incorporated in Delaware, and our offices and laboratory facilities are located in Smyrna, Georgia (metropolitan Atlanta).the target infection should it appear.

Our current development programs are focused on vaccines are being evaluatedagainst Human Immunodeficiency Virus (HIV) and hemorrhagic fever viruses (Ebola, Marburg). We believe our technology and vaccine development expertise is well-suited for a variety of human infectious diseases and, potentially, cancer immunotherapy. We intend to determine their potential to (a) prevent HIV infection and (b) to serve as a treatment for individuals who are already infected with HIV. These vaccines are currently being evaluated in human clinical trials.pursue expansion of our product pipeline.

Our most advanced vaccines under development are designed to function againstHIV vaccine program is focused on the clade B subtype of the HIV virus that is prevalent in the Americas and westernWestern Europe. An estimated 3.3 million people are infected withOur preventive clade B HIV virus worldwide, with 187,000 new infectionsvaccine has successfully completed Phase 2a human clinical testing and is targeted to enter a follow-on clinical trial in 2012,early 2016. It has shown outstanding safety and excellent and highly reproducible immunogenicity (Journal of which 51,000 were in the United States. The cost of treating HIV-infected individuals in the U.S. is estimated at $500,000 for each infected individual over their lifetime.

SubjectInfectious Diseases volume 203, pg 610 and volume 210 pg 99). We are also extending our HIV vaccine effort to the availability of funding support from governmental or nongovernmental organizations, we also planmost common virus subtype affecting sub-Saharan Africa, clade C and are conducting preclinical studies pursuant to develop vaccines designed for use to combat the subtypes of HIV that predominate in the developing countries. We have licenseda grant from the NIH the MVA constructNational Institutes of Health (NIH). Additionally, we are investigating our HIV vaccines for the clade C subtype oftheir potential to contribute to combination therapies for therapeutic treatment leading to a cure for HIV prevalent in South Africa and India, and have begun early development work on a vaccine for this subtype of the virus.infections.

Our hemorrhagic fever vaccine program was initiated during 2014 with the objective of developing both monovalent vaccines incorporate two delivery components:and tetravalent vaccines designed to protect not only against current strains for filoviruses such as Ebola and Marburg, but also against other major hemorrhagic fever viruses endemic in African countries. Studies of our first Ebola vaccine candidate have demonstrated 100 percent protection in rodent models. We plan to conduct additional animal challenge studies during 2016 with the goal of beginning human clinical trials during the first half of 2017.

In December 2015, we entered into a recombinant DNACollaborative Research Agreement with the University of Pittsburgh to evaluate our VLP vaccine platform for use in cancer immunotherapy, including the selection and a recombinant poxvirus designated modified vaccinia Ankara (MVA) vaccine. Bothtesting of vaccine candidates.

Our vaccine development activities have been, and continue to be, financially supported by the DNA and MVA vaccines contain sufficient HIV genes toU.S. government. This support has been both in the production of non-infectious virus-like particles.  These particles display the native trimeric-membrane-bound form of research grants awarded directly to us, as well as indirect support for the viral envelope glycoprotein that mediates entry into cells and is the target for protective antibody. When used together, the recombinant DNA component primes immune responses, which are boosted by administration of the recombinant MVA component. We have also tested an adjuvanted versionconduct of our vaccine that co-expresses granulocyte-macrophage colony-stimulating factor (GM-CSF) inhuman clinical trials. This is discussed further under “Support from the DNA vaccine used to prime the immune response. An adjuvant is an agent that can improve a vaccine response.United States Government” below.

Work on our vaccines began during the 1990s at Emory University in Atlanta, Georgia, under the direction of Dr. Harriet L. Robinson, who is now our Chief Scientific Officer.

Our HIV vaccine technology was developed in collaboration with researchers at Emory University, the NIH, and the CDC.Centers for Disease Control and Prevention (CDC). The technology developed by the collaboration is exclusively licensed to us from Emory University. We also have nonexclusive licenses to certain patents owned by the NIHNIH. Our Ebola/Marburg vaccines have been developed with technology licensed from, and exclusive license rights to certain manufacturing process patentsin collaboration with, the NIH.

Each of MFD, Inc.our vaccine development programs is discussed in greater detail in the sections that follow below.

Therapeutic HIV Vaccine Program

A Phase 1 clinical trial (GV-TH-01) investigating the therapeutic use ofWe are incorporated in Delaware, and our HIV vaccine is nearing completion,offices and we expect to release final results in the first quarter of 2014. The primary endpoint of this 9 patient “treatment interruption” study is to evaluate the safety of our vaccine in HIV-positive patients with well-controlled infections who are being treated with oral HIV medications. An exploratory objective of the study is to evaluate the ability of the vaccinated patient to control re-emergent virus during a 12-week period of drug treatment interruption in which patients are removed from their anti-retroviral medications.

In a follow-on study, we are formulating plans for a Phase 1 clinical trial investigating the treatment of HIV-positive individuals with our vaccine in combination with standard-of-care antiretroviral drug therapy. The primary and secondary objectives of the study will be to evaluate the safety and immunogenicity of our DNA/MVA vaccine. An exploratory objective will be to investigate the vaccine’s effect on reducing viral reservoirs. We plan to submit a grant proposal to the NIH for financial support to conduct this trial which, if accepted, would allow us to begin in mid-2015. If we are able to secure sufficient capital from issuance of our equity securities or other sources, we may be able to initiate this trial sooner.

Preventive HIV Vaccine Program

Clinical trials of our preventive vaccine have been conducted by the HIV Vaccine Trials Network. The HIV Vaccine Trials Network (HVTN) is the largest worldwide clinical trials network dedicated to the development and testing of HIV/AIDS vaccines. Support for the HVTN comes from the National Institute of Allergy and Infectious Diseases (NIAID), part of the U.S. National Institutes of Health (NIH). The HVTN’s HIV Vaccine Trial Unitslaboratory facilities are located at leading research institutions in 27 cities on four continents.

HVTN 065, a 120 person first in humans Phase 1 trial of our JS7 DNA prime and MVA62B boost showed good safety and immunogenicity and supported moving to Phase 2 testing. HVTN 205, a 300 person Phase 2a trial for MVA62B with or without a JS7 DNA prime has been completed. Participants received either 2 doses of JS7 DNA vaccine followed by 2 doses of MVA/HIV62B at 0, 2, 4, and 6, months (DDMM regimen), 3 doses of MVA/HIV62B at 0, 2, and 6 months (MMM regimen) or placebo injections. At peak response, 93.2% of the DDMM group and 98.4% of the MMM group had binding antibodies (Ab) for the envelope glycoprotein (Env) Smyrna, Georgia (metropolitan Atlanta). These binding Abs were more frequent and of higher magnitude for the transmembrane (gp41) than the receptor binding subunit (gp120) of the HIV envelope glycoprotein (Env).For both regimens, response rates were higher for CD4+ (66.4% DDMM, 43.1% MMM) than CD8+ (21.8% DDMM, 14.9% MMM) T cells. Responding CD4+ and CD8+ T cell were biased towards Gag and >70% produced two, or three, of four tested cytokines. At 6 months post vaccination, the magnitudes of Ab and T cell responses had decreased by <3- fold. These results distinguished our vaccine from other vaccines that have advanced to efficacy testing in the specificity and durability of elicited antibody responses. The durability of the Ab responses is important because protection waned with the waning Ab response in the one partially successful HIV vaccine trial, RV144 conducted by the US military and the Thai government in Thailand.

An ongoing Phase 1 clinical trial (HVTN 094) using the adjuvanted version of our vaccine (GOVX-BO2) has proven to be no more effective than the non-adjuvanted form of the vaccine (GOVX-BO1) in eliciting immune responses in humans. Comparison of data between HVTN 094 and HVTN 205 did not show a benefit for adding the adjuvant to the vaccine. HVTN 094 did address adding a third MVA boost to our formerly two MVA boost regimen and allowing a longer interval between the last two MVA inoculations. On the basis of the data obtained with the 3^rd MVA boost, we anticipate that a DDMMM regimen of GOVX-BO1 with a 4 month interval before the last inoculation will advance into efficacy trials in at-risk individuals. 

Background – Viruses and Vaccines

WhatOur Technology

Vaccines typically contain agents (antigens) that resemble disease-causing microorganisms. Traditional vaccines are Viruses? Virusesoften made from weakened or killed forms of the virus or from its surface proteins. Many newer vaccines use recombinant DNA (deoxyribonucleic acid) technology to generate vaccine antigens in bacteria or cultured cells from specific portions of the DNA sequence of the target pathogen. The generated antigens are microscopic organisms consistingthen purified and formulated for use in a vaccine. The most successful of genetic material comprised ofthese purified antigens have been non-infectious virus-like particles (VLPs) as exemplified by vaccines for hepatitis B (Merck’s Recombivax® and GSK’s Engerix®) and Papilloma viruses (GSK’s Cervarix®, and Merck’s Gardasil®). Our approach uses recombinant DNA or ribonucleic acid (“RNA”), surrounded by a protein, lipid (fat), or glycoprotein coat. Viruses invade healthy, living hostrecombinant viruses to produce VLPs in the person being vaccinated. In human clinical trials of our HIV vaccines, we have demonstrated that our VLPs, expressed in the cells of the person being vaccinated, are safe, yet elicit both strong and durable humoral and cellular immune response.

All of our vaccines are designed to produce self-assembling non-infectious VLPs in order to replicate and spread. In many cases,the cells of the person being vaccinated. VLPs train the body’s immune system canto recognize and effectively combatkill the authentic virus should it appear. VLPs also train the immune system to recognize and kill infected cells to control infection and reduce the length and severity of disease. One of the biggest challenges with VLP-based vaccines is to design the vaccines in such a way that the VLPs will be recognized by the immune system in the same way as the authentic virus would be. When VLPs for enveloped viruses like HIV, Ebola, and Marburg are producedin vivo, they include not only the protein antigens, but also an infection causedenvelope consisting of membranes from the vaccinated individual’s cells. In this way, they are highly similar to the virus generated in a person’s body during a natural infection. VLPs produced externally, by a virus. However, with certain viral infections,contrast, have no envelope; or, envelopes from the cultured cells (typically hamster or insect cells) used to produce them. We believe our technology provides distinct advantages by producing VLPs that more closely resemble the authentic virus, which in turn, allows the body’s immune system is unable to fully destroy or inhibitmore readily recognize the replicationauthentic virus. By producing VLPsin vivo, we avoid potential purification issues associated within vitro production of the virus, which results in persistent and ongoing viral replication resulting in disease.VLPs.

Infections causedDNA and MVA as Vaccine Vectors.Our HIV vaccines incorporate two delivery components (or vectors): a recombinant plasmid DNA vaccine, and a recombinant MVA (modified vaccinia Ankara) vaccine. Our Ebola and Marburg vaccines use only the MVA vector. Both our DNA and MVA vaccines express sufficient vaccine genes to support the production of non-infectious VLPs. The VLPs cannot cause disease because they contain mutated or deleted enzymatic functions that are essential for virus replication. The virus-like particles display trimeric membrane bound forms of the viral envelope glycoprotein (Env for HIV or GP for Ebola or Marburg). This is important because the natural form of the envelope glycoprotein elicits multi-target antibody capable of recognizing incoming virus and blocking infections. Expression of multiple proteins by viruses can be chronic or acute. Chronic infections,the vaccines is essential for the formation of VLPs. The multiple proteins also provide more targets for immune responses such as those caused by HIV, do not typically self-resolve with timecytotoxic T-cells. Elicitation of multi-target humoral and can cause chronic disease. Acute infections associated with viruses, suchcellular responses limits immune escape, just as influenza, generally last for a relatively short period of time, and self-resolve in most immuno-competent individuals.

Viruses can also be characterized as either active or latent. An active virus can cause a persistent infection or disease over an extended period of time. A latent virus will remain in the body for very long periods of time after the initial infection and generally will only cause disease when the body’s immune system weakens, fails or is suppressed, allowing the virus to once again replicate. Vaccines have been widely used to prevent active viral infections from occurring.

Viruses that develop resistance to antiviral drugs are increasingly becoming a challenge in the treatment of viral infections, particularly those that are chronic in nature. The ability of viruses to mutate spontaneously during replication allows drug-resistant strains to emerge when patients are using drugs that are not potent enough to quickly and completely inhibit viral replication. Drug resistance occurs because viruses continually replicate making millions of copies of themselves, some of which contain mutations in their genetic material. Mutations that emerge in the presence of a suppressive antiviralmulti-drug therapies limit drug will give rise to mutant strains that are wholly or partially resistant to that drug. These mutant viruses, while initially low in number, eventually become the predominant strain in an infected patient as those strains that remain susceptible to the drug are inhibited from replicating. Once this occurs, the treatment benefit of that particular antiviral drug often diminishes, resulting in treatment failure and the need for an alternate therapy with different or possibly new drugs, or classes of drugs. In general, viruses that cause chronic infections, such as HIV, are more likely to develop drug resistance due to the long-term and persistent exposure of the virus to the antiviral therapy.escape.

Ebola VLPs                                                     HIV VLPs

What are Vaccines?Figure 1. Electron micrographs showing the virus-likeparticles (VLPs) elicited by GeoVax vaccines from human cells. Vaccines represent an approach to broadenNote that the ability to prevent serious infectious diseases caused by both viruses and bacteria.A vaccine is a substance introducedEbola VLPs on the left self-assemble into the human body that teaches the immune system to detect and destroy a pathogen (a virus or bacterium that causes disease). All vaccines contain some harmless form or partrod-like shape of the pathogen they target. They exert their effects throughauthentic Ebola virus, while the adaptive immune response, an armHIV VLPs shown on the right take on the spherical shape of the authentic HIV virus. While below the resolution of these micrographs, both types of VLPs display what we believe to be the native form of their respective viral envelope glycoproteins which we believe is key to generating an effective immune system that learns to recognize and neutralize specific pathogens.humoral response.

There are several typesWe selected MVA for use as the live viral component of vaccines:

Overview of HIV/AIDS

What is HIV?HIV is a retrovirus that carries its genetic code in the form of RNA. Retroviruses use RNA and the reverse transcriptase enzyme to create DNA from the RNA template. The HIV-1 virus invades human cells and produces its viral DNA that is subsequently inserted into the chromosomes, which are the genetic material of a cell. HIV preferentially infects and replicates in T-cells, which are a type of white blood cell. Infection of T-cells alters them from immunity mediating cells to cells that produce and release HIV. This process results in the destruction of the immune defense systemability of infected individuals and ultimately, the development of AIDS.

There are several AIDS-causing HIV virus subtypes, or clades, that are found in different regions of the world. These clades are identified as clade A, clade B and so on. The predominant clade found in Europe, North America, parts of South America, Japan and Australia is clade B, whereas the predominant clades in Africa are clades A and C. In India, the predominant clade is clade C. Each clade differs by at least 20% with respectthis vector to its genetic sequence from other clades. These differences may mean that vaccines or treatments developed against HIV of one clade may only be partially effective or ineffective against HIV of other clades. Thus, there is often a geographical focus to designing and developing vaccines suited for the local clade.

HIV, even within clades, has a high rate of mutation that supports a significant level of genetic variation. In drug treatment programs, virus mutation can result in the development of drug resistance, referred to as virus drug escape, thereby rendering drug therapy ineffective. Hence, we believe that multi-drug therapy is very important. If several drugs are active against virus replication, the virus must undergo multiple simultaneous mutations to escape, which is less likely. The same is true for immune responses. HIV can escape single targeted immune responses. However, our scientists believe if an immune response is directed against multiple targets, which are referred to as epitopes, virus escape is much less frequent. Vaccination against more than one of the proteins found in HIV increases the number of targets for the immune response as well as the chance that HIV will not escape the vaccine-stimulated immune response, thus resulting in protection against infection or the development of clinical AIDS once infection occurs.

What is AIDS? AIDS is the final, life-threatening stage of infection with the virus known as HIV. Infection with HIV severely damages the immune system, the body’s defense against disease. HIV infects and gradually destroys T-cells and macrophages, which are white blood cells that play key roles in protecting humans against infectious disease caused by viruses, bacteria, fungi and other micro-organisms.

Opportunistic infections by organisms, normally posing no problem for control by a healthy immune system, can ravage persons with immune systems damaged by HIV infections. Destruction of the immune system occurs over years. The average onset of the clinical disease recognized as AIDS occurs after three to ten years of HIV infection if the virus is not treated effectively with drugs, but the time to developing AIDS is highly variable.

AIDS in humans was first identified in the United States in 1981, but researchers believe that it was present in Central Africa as early as 1959. AIDS is most often transmitted sexually from one person to another but it is also transmitted by blood in shared needles and through pregnancy and childbirth. Heterosexual activity is the most frequent route of transmission worldwide.

The level of virus in blood, known ascarry sufficient viral load, is the best indicator of the speed with which an individual will progress to AIDS and the frequency with which an individual will spread infection. An estimated 1% or fewer of those infected have low enough levels of the virus to preclude progression to AIDS and to not transmit the infection. These individuals are commonly called elite controllers or long-term non-progressors.

AIDS is considered by many in the scientific and medical community to be the most lethal infectious disease in the world. According to the report published by UNAIDS/WHO, at the end of 2012, an estimated 36 million people were living with HIV worldwide, with approximately 2.5 million newly infected in 2012 alone. Approximately 25 million people infected with HIV have died since the 1981 start of the HIV pandemic. The United States currently suffers about 51,000 infections per year, of which only an estimated 25% enter into, and maintain, successful drug treatment.

At present, the standard approach to treating HIV infection is to inhibit viral replication through the use of combinations of drugs. Available drugs include reverse transcriptase inhibitors, protease inhibitors, integration inhibitors and inhibitors of cell entry to block multiple essential steps in virus replication. However, HIV is prone to genetic changes that can produce strains that are resistant to currently approved drugs. When HIV acquires resistance to one drug within a class, it can often become resistant to the entire class, meaning that it may be impossible to re-establish control of a genetically altered strain by substituting different drugs in the same class. Furthermore, these treatments continue to have significant limitations which include toxicity, patient non-adherence to the treatment regimens and cost. As a result, over time, many patients develop intolerance to these medications or simply give up taking the medications due to the side effects.

According to the International AIDS Vaccine Initiative (IAVI), the cost and complexity of new treatment advances for AIDS puts them out of reach for most people in the countries where treatment is most needed, and as noted above, in industrialized nations, where drugs are more readily available, side effects and increased rates of viral resistance have raised concerns about their long term use. AIDS vaccines, therefore, are seen by many as the most promising way to end the HIV/AIDS pandemic. It is expected that vaccines for HIV/AIDS, once developed, will be used universally and administered worldwide by organizations that provide health care services, including hospitals, medical clinics, the military, prisons and schools.

Our Vaccine Candidates

Our vaccines, initially developed by our Chief Scientific Officer, Dr. Harriet L. Robinson at Emory University in collaboration with scientists at the NIH and the CDC, incorporate two vaccine delivery components: (1) a recombinant DNA (deoxyribonucleic acid) and (2) a recombinant poxvirus, known as MVA (modified vaccinia Ankara), both of which deliver genes that encode inactivated HIV derived proteins to the immune system. Both the DNA andproduce virus-like particles. MVA vaccines contain sufficient HIV genes to support the production of non-infectious virus-like particles which display the native trimeric membrane-bound form of the viral envelope glycoprotein that appears authentic to the immune system. When used together, the recombinant DNA component is used to prime the immune response, which is then boosted by administration of the recombinant MVA component. However, in certain settings the recombinant MVA alone may be sufficient for priming and boosting the immune responses.

Our initial work focused on the development ofwas originally developed as a preventivesafer smallpox vaccine for use in uninfected humansimmune compromised humans. It was developed by attenuating the standard smallpox vaccine by making over 500 passages of the virus in chicken embryos or chick embryo fibroblasts, which resulted in a virus with limited ability to prevent infection should they be exposedreplicate in human cells but did not compromise the ability of MVA to grow on avian cells, which are used for manufacturing the virus. Later, based on encouraging data in preclinical primate models, we undertook the development of a therapeutic vaccine for use in HIV infected humans to supplement approved drug regimens. For both preventive and therapeutic applications, our primary focus is on a vaccine for use against clade B, which is commonThe deletions also resulted in the United States andloss of immune evasion genes which assist the industrially developed world. However, if efficacy is documented against clade B, we planspread of wild type smallpox infections, even in the presence of human immune responses. MVA was safely administered to develop vaccines designed for use to combatover 120,000 people in the subtypes of HIV that predominate in developing countries, including clades A, C and an AG recombinant.We have licensed from the NIH the MVA construct for the clade C version of HIV prevalent in South Africa and India, and have begun early development work on1970s as a vaccine for this subtype of the virus.smallpox vaccine.

Induction of T-cell and Antibody Immune Responses.In both preclinical and clinical trials, our HIV vaccines have been shown to induce both anti-viral antibodyhumoral (antibody) and T-cell responses.cellular (T-cell) responses against HIV. The induction of both antibodies and T-cells is beneficial because these immune responses work through different mechanisms. Antibodies can prevent infection by blocking viruses from infecting cells. In preclinical simian vaccine studies using repeated rectal challenges with moderate doses of virus, the avidity, or tightness, of antibody binding to the surface envelope glycoprotein of HIV correlates with the prevention of infection (The Journal of Infectious Diseases,204:164 (2011)). In high dose challenges that infect all animals at the first exposure, the avidity of the antibody for envelope glycoprotein correlates with reduced levels of virus replication (Journal of Virology, 83:4102 (2009)). Similarly, antibody responses are believed to be critical for vaccine-elicited protection against Ebola and Marburg infection (Expert Review of Vaccines, 10:63 (2011)). These results likely reflect the tightly binding antibody both blocking infection as well as tagging the virus and infected cells for destruction, by white blood cells such as macrophages, neutrophils and natural killer cells. Our vaccines elicit CD8CD8+ T-cells, a type of T-cell that can recognize and kill cells that become infected by virus (without antibody tagging). CD8For HIV, CD8+ T-cells are important for the control of the virus that has established an infection.  For Ebola and Marburg, antibodies can stop or slow the progress of infection, but T cells are important for clearing the infection by killing remaining infected cells.

Background – Viruses and Vaccines

What are Viruses? Viruses are microscopic organisms consisting of genetic material comprised of DNA (deoxyribonucleic acid) or RNA (ribonucleic acid), surrounded by a protein, lipid (fat), or glycoprotein coat. Viruses invade healthy, living host cells in order to replicate and spread. In many cases, the body’s immune system can recognize and effectively combat an infection caused by a virus. However, with certain viral infections, the body’s immune system is unable to fully destroy or inhibit the replication of the virus, which results in persistent and ongoing viral replication resulting in disease.

Infections caused by viruses can be chronic or acute. Chronic infections, such as those caused by HIV, do not typically self-resolve with time and can cause chronic disease. Acute infections associated with viruses, such as influenza, generally last for a relatively short period of time, and self-resolve in most immunocompetent individuals. However, certain acute infections, such as those caused by Ebola and Marburg, can overwhelm the immune system, resulting in serious disease and death.

Viruses can also be characterized as either active or latent. An active virus can cause a persistent infection or disease over an extended period of time. A latent virus will remain in the body for very long periods of time after the initial infection and generally will only cause disease when the body’s immune system weakens, fails or is suppressed, allowing the virus to once again replicate. Vaccines have been widely used to prevent active viral infections from occurring. Latent infections are more difficult to address with vaccines. A latent virus does not replicate actively and can “fly below the radar” of the immune system in that it does not provide the immune system with targets for antibody and T-cell responses.

Viruses that develop resistance to antiviral drugs are increasingly becoming a challenge in the treatment of viral infections, particularly those that are chronic in nature. The ability of viruses to mutate spontaneously during replication allows drug-resistant strains to emerge when patients are using drugs that are not potent enough to quickly and completely inhibit viral replication. Drug-resistant mutant viruses, while initially low in number, eventually become the predominant strain in an infected patient as those strains that remain susceptible to the drug are inhibited from replicating. Once this occurs, the treatment benefit of that particular antiviral drug diminishes, resulting in treatment failure and the need for an alternate therapy with different or possibly new drugs, or classes of drugs. In general, viruses that cause chronic infections, such as HIV, are more likely to develop drug resistance due to the long-term and persistent exposure of the virus to the antiviral therapy.

What are Vaccines? Vaccines represent an approach to broaden the ability to prevent serious infectious diseases caused by both viruses and bacteria.A vaccine is a substance introduced into the human body that teaches the immune system to detect and destroy a pathogen (a virus or other pathogen that causes disease). All vaccines contain some harmless form or part of the pathogen they target or of a highly similar pathogen. They exert their effects through the adaptive immune response, an arm of the immune system that learns to recognize and control specific pathogens.

There are several types of vaccines:

Our Ebola & Marburg Vaccine Program

About Ebola and Marburg. Ebola Hemorrhagic Fever (EHF) and the related disease Marburg Virus Disease (MVD) are highly contagious, extremely deadly diseases that, if not contained by quarantine, are capable of threatening populations worldwide. Since 1976, when Ebola was first discovered, at least 28 outbreaks have occurred. The 2014 Ebola outbreak in West Africa was significantly larger than any previous epidemic, the first to reach urban areas and the first to lead to person-to-person transmission in the United States. This outbreak resulted in approximately 28,600 infections with over 11,000 deaths (40% fatality rate). No approved preventive or therapeutic products exist for EHF or MVD.

Ebola and Marburg naturally infect animals including bats, creating reservoirs of Ebola and Marburg that, like rabies, cannot be completely eradicated. The rapid urbanization of many areas of Sub-Saharan Africa and the ease of modern air travel create conditions that facilitate the epidemic spread of EHF and MVD, which previously had been limited to localized outbreaks in villages. EHF is caused by ebolaviruses (Ebola), and MVD is caused by marburgviruses (Marburg). Ebola and Marburg are members of the familyFiloviridae. Ebolaviruses are more diverse than marburgviruses and are divided into five subtypes: Zaire, Sudan, Bundibugyo, Tai Forest, and Reston. Zaire is the most lethal of the strains and is responsible for the current epidemic. Sudan and Bundibugyo are also lethal but have caused fewer and less severe outbreaks.

A challenge in Ebola and Marburg vaccine development is the need to create products that are effective both in containing an epidemic (in which rapid responses are critical) and in routine immunization (in which the duration of immunity is important). Ideal countermeasures to Ebola and Marburg would include a single-shot strain-specific epidemic vaccine capable of rapidly producing protective antibodies and T cells, and a routine vaccine capable of eliciting durable immunity to the lethal strains of Ebola (Zaire, Sudan and Bundibugyo) as well as Marburg. An effective vaccine against Ebola and/or Marburg would dramatically reduce the epidemic spread of infections as well as the transmission of Ebola and/or Marburg from natural animal hosts to humans.

Research on Ebola vaccines is progressing rapidly amongst a number of different pharmaceutical companies, with recombinant chimpanzee adenovirus (ChAd3), rare-serotype adenovirus (Ad26) and vesicular stomatitis virus (VSV) candidates already in clinical trials and several other vaccines scheduled to begin clinical trials. However, none of these vaccines has an ideal design, nor are any of them well suited for use in proactive immunization of populations to prevent future epidemics. The adenovirus vaccines require boosting with MVA to raise protective immune responses, and the two-product regimen (adenovirus and MVA) dramatically raises manufacturing costs and the complexity of vaccination. The replication competent VSV recombinants have already shown risk signals in the current trial, necessitating a temporary halt to the trial followed by resumption at a lower vaccine dose. The potential dose-limiting toxicity of the VSV vaccines raises safety concerns for large-scale vaccinations and also could pose threats to immunocompromised people, such as those infected with HIV. None of the competitors’ vaccines produce virus-like particles, a desirable characteristic, which is discussed in detail elsewhere in this document. To the best of our knowledge, no non-GeoVax vaccine candidates share this characteristic. One or more of the current candidates may well show success in stemming the current epidemic. However, the world must be prepared with the optimal vaccine for the next epidemic when it occurs. All of the vaccines currently in clinical trials are designed to protect against one, or at most two, strains of Ebola. To be successful, an optimal vaccine should be safe, effective, and long lasting, all at a reasonable cost. Our analysis suggests that the GeoVax designs are well suited to achieve this aim.

Our Vaccines. To address the unmet need for a product to prevent hemorrhagic fever viruses, we are developing a series of vaccines, which combine our proven MVA technology with advanced vaccine design. We are developing individual vaccines (monovalent) that will address each of the lethal strains of Ebola virus (Zaire, Sudan and Bundibugyo), as well as Marburg virus. We also are developing a multivalent vaccine, which will incorporate multiple monovalent vaccines to protect not only against current strains of filoviruses such as Ebola and Marburg, but also against other major hemorrhagic fever viruses endemic in African countries.

In April 2015, we entered into a Research Collaboration Agreement with the National Institute of Allergy and Infectious Diseases (NIAID), part of the NIH, for development of our vaccines against Ebola and Marburg viruses. Under this agreement, NIAID is contributing materials, reagents, and scientific advice for vaccine construction, and has conducted animal protection studies in guinea pigs, and hamsters. In September, studies of our first Ebola vaccine candidate conducted pursuant to this collaboration demonstrated 100 percent protection in these small animal models. We plan to conduct additional animal challenge studies during 2016 with the goal of beginning human clinical trials during the first half of 2017. We intend to seek additional funding from U.S. government agencies and/or world health organizations to assist us in this regard.

We believe our Ebola/Marburg vaccines will demonstrate a unique combination of advantages that set them apart from any other products in development for prevention of EHF.

Our HIV/AIDS Vaccine Vectors.Program

About HIV/AIDS.HIV is a retrovirus that carries its genetic code in the form of RNA. Retroviruses use RNA and the reverse transcriptase enzyme to create DNA from the RNA template. The HIV-1 virus enters human cells and copies its viral RNA to produce complementary DNA (cDNA) that is subsequently inserted into the chromosomes, which are the genetic material of a cell. HIV preferentially infects and replicates in T-cells, which are a type of white blood cell. Infection of T-cells alters them from immunity mediating cells to cells that produce and release HIV. This process results in the destruction of the immune defenses of infected individuals and ultimately, the development of AIDS.

There are several AIDS-causing HIV virus subtypes, or clades, that are found in different regions of the world. These clades are identified as clade A, clade B and so on. The predominant clade found in Europe, North America, parts of South America, Japan and Australia is clade B, whereas the predominant clades in Africa are clades A and C. In India, the predominant clade is clade C. Each clade differs by at least 20% with respect to its genetic sequence from other clades. These differences may mean that vaccines or treatments developed against HIV of one clade may only be partially effective or ineffective against HIV of other clades. Thus, there is often a geographical focus to designing and developing HIV vaccines.

HIV, even within clades, has a high rate of mutation that supports a significant level of genetic variation. In drug treatment programs, virus mutation can result in the development of drug resistance, referred to as virus drug escape, thereby rendering drug therapy ineffective. Hence, we believe that multi-drug therapy is very important. If several drugs are active against virus replication, the virus must undergo multiple simultaneous mutations to escape, which is less likely. The same is true for immune responses. HIV can escape single targeted immune responses. However, our scientists believe if an immune response is directed against multiple targets, which are referred to as epitopes, virus escape is much less frequent. Vaccination against more than one of the proteins found in HIV increases the number of targets for the immune response as well as the chance that HIV will not escape the vaccine-stimulated immune response, thus resulting in protection against infection or the development of clinical AIDS if infection occurs.

HIV infects and gradually destroys T-cells and macrophages, which are white blood cells that play key roles in protecting humans against infectious disease caused by viruses, bacteria, fungi and other micro-organisms. Opportunistic infections by organisms, normally posing no problem for control by a healthy immune system, can ravage persons with immune systems damaged by HIV infections. Destruction of the immune system occurs over years. The average onset of the clinical disease recognized as AIDS occurs after three to ten years of HIV infection if the virus is not treated effectively with drugs, but the time to developing AIDS is highly variable.

AIDS is considered by many in the scientific and medical community to be the most lethal infectious disease in the world. An estimated 37 million people are living with HIV worldwide, with approximately 2.5 million newly infected in 2012 alone. Approximately 39 million people infected with HIV have died since the 1981 start of the HIV pandemic. The United States currently has an estimated 1.2 million HIV-infected individuals, with approximately 50,000 new infections per year.

At present, the standard approach to treating HIV infection is to inhibit viral replication through the use of combinations of drugs. Available drugs include reverse transcriptase inhibitors, protease inhibitors, integration inhibitors and inhibitors of cell entry to block multiple essential steps in virus replication. However, HIV is prone to genetic changes that can produce strains that are resistant to currently approved drugs. When HIV acquires resistance to one drug within a class, it can often become resistant to the entire class, meaning that it may be impossible to re-establish control of a genetically altered strain by substituting different drugs in the same class. Furthermore, these treatments continue to have significant limitations which include toxicity, patient non-adherence to the treatment regimens and cost. As a result, over time, viruses acquire drug-resistant mutations, and many patients develop intolerance to the medications or simply give up taking the medications due to the side effects.

According to the International AIDS Vaccine Initiative (IAVI), the cost and complexity of new treatment advances for AIDS puts them out of reach for most people in the countries where treatment is most needed. As noted above, in industrialized nations, where drugs are more readily available, side effects and increased rates of viral resistance have raised concerns about their long term use. AIDS vaccines, therefore, are seen by many as the most promising way to end the HIV/AIDS pandemic. It is expected that vaccines for HIV/AIDS, once developed, will be used universally and administered worldwide by organizations that provide health care services, including hospitals, medical clinics, the military, prisons and schools.

Our Preventive HIV Vaccine Program

Prevention of HIV infection remains a worldwide unmet medical need, even in the United States and other first world countries where effective antiretroviral therapies are available. There is no approved HIV vaccine. Current antiretroviral therapies do not eliminate HIV infection, requiring individuals to remain on antiretroviral drugs for their entire lives. In the United States, it is estimated that of the 1.2 million infected individuals, for various reasons (lack of diagnosis, linkage to care, patient compliance, etc.) only 25% ultimately remain in HIV care with their viral load sufficiently suppressed to prevent spread of HIV. As a result, the annual incidence of new HIV infections has remained virtually unchanged for the past 20 years. Furthermore, the annual financial burden to the U.S. taxpayer for HIV education, prevention, and treatment costs borne through multiple federal agencies is more than $20 billion annually.

Work on our HIV vaccines began during the 1990s at Emory University in Atlanta, Georgia, under the direction of Dr. Harriet L. Robinson, who is now our Chief Scientific Officer. The vaccine technology was developed in collaboration with researchers at the NIH and the CDC.

Our most clinically advanced vaccine development program is a DNA/MVA vaccine regimen designed to protect against the clade B subtype of the HIV virus. Clade B is prevalent in the Americas and Western Europe. An estimated 3.3 million people are infected with clade B HIV virus worldwide, with 187,000 new infections in 2012.

We have two HIV vaccine components under development: a recombinant DNA vaccine, and a recombinant MVA vaccine. Both the DNA and MVA vaccines producecontain sufficient HIV genes to support the production of non-infectious virus-like particles containingparticles.  These VLPs display the three major proteins of HIV. The virus-like particles cannot cause disease because they were designed with mutated or deleted enzymatic functions that are essential for virus replication.  The virus-like particles displaynative trimeric membrane bound formsmembrane-bound form of the HIV envelope glycoprotein (Env). This that mediates entry into cells and is important because the natural formtarget for protective antibody. When used together, the recombinant DNA component primes immune responses, which are boosted by administration of the envelope glycoproteinrecombinant MVA component. This prime-boost strategy elicits antibody capablehigh avidity antibodies (tightly binding antibodies) and cytotoxic T cells. The antibodies can block infections and initiate the killing of recognizing incoming virus and blocking infections. Expressioninfected cells by bound antibody signaling destruction by virion capture, antibody-dependent cellular cytotoxicity, phagocytosis and complement mediated lysis. We may also pursue development of multiple proteinsour MVA vaccine component as a standalone HIV vaccine, or in combination with other vaccine components.

Clinical trials of our preventive HIV vaccine have been conducted by the HIV Vaccine Trials Network (HVTN). The HVTN is the largest worldwide clinical trials network dedicated to the development and testing of HIV/AIDS vaccines. Support for the HVTN comes from the National Institute of Allergy and Infectious Diseases (NIAID), part of the NIH. The HVTN’s HIV Vaccine Trial Units are located at leading research institutions in 27 cities on four continents.

We have completed multiple Phase 1 trials and a Phase 2a trial (HVTN 205) of various dosing regimens and formulations of our vaccines. These vaccines have been evaluated in nearly 500 humans. All of the clinical trials of our preventive vaccines have been conducted by the HVTN, and fully funded by the NIH.

We also expect the NIH to fully fund the cost of another Phase 1 trial (HVTN 114) of our preventive HIV vaccine to begin in early 2016, which will investigate the effect of adding a “protein boost” component to our vaccine. Protein boosts may augment antibody responses that can block virus infections (neutralizing antibody) and cause antibody dependent cellular cytotoxicity (ADCC antibody). Proteins added to HIV vaccines have shown some success in other trials. The HVTN believes this “dual-action” approach will be a prudent and cost-effective path forward for supporting large clinical trials. Information from this trial would then inform the design of future, larger clinical trials. While efforts are underway to evaluate the protein boost concept, we also intend to seek funding to expedite our vaccine (without the additional protein boost) directly into pivotal Phase 2b efficacy trials.

The HVTN is important because each protein provides targetscontinuing to consider future efficacy studies, and members are working to develop collaborative clinical development plans, as well as initiating regulatory planning. The plans for cytotoxic T-cells. Elicitation of a multi-target T-cell response limits immune escape, justlarge-scale clinical trials may change as multi-drug therapies limit drug escape.researchers continue to gather information from our earlier studies and are influenced by results from other vaccine trials. Trial start dates are dependent on many factors and are likely to change.

MVA was selectedPreventive HIV Vaccine Program – Clade C. We also plan to develop vaccines designed for use asto combat the live viral componentsubtypes of our vaccines becauseHIV that predominate in the developing countries. We have licensed from the U.S. National Institutes of its well established safety recordHealth (NIH) the modified vaccine Ankara (MVA) construct for the clade C subtype of HIV prevalent in South Africa and becauseIndia, and we have completed lead discovery using a novel approach to vaccination against clade C. We have performed initial process development studies for the NIH-developed vaccine and initiated early development work on the other, newer clade C vaccine. Depending on the results of animal studies and the focus of future government support, we may advance either or both of the abilityclade C vaccines into the clinic. In June 2015, the NIH awarded us a Small Business Innovative Research (SBIR) grant entitled “Directed Lineage Immunizations for Eliciting Broadly Neutralizing Antibody” toward this effort. The initial grant award of this vector to carry sufficient HIV proteins to produce virus-like particles. MVA was originally developed as$299,585 is for the first year of a safer smallpox vaccine for use in immune compromised humans.  It was developed by attenuating the standard smallpox vaccine by making over 500 passages of the virus in chicken embryos or chick embryo fibroblasts which resulted in large genomic deletions. These deletions limited the ability of MVA to replicate in human cells, which can cause safety problems, but did not compromise the ability of MVA to grow on avian cells that are used for manufacturing the virus. The deletions also resulted in the loss of immune evasion genes which assist the spread of wild type smallpox infections, even in the presence of human immune responses. MVA was safely administered to over 120,000 people in the 1970s as a smallpox vaccine.two year project period beginning July 1, 2015.

Preclinical Studies.During the developmentWe conducted preclinical efficacy trials of our preventive HIV vaccines preclinical efficacy trials were conducted by vaccinating non-human primates with simian immunodeficiency virus prototypes of our HIV vaccines and then testing them for resistance to simian immunodeficiency virus infection. The experimental data produced by these trials documented the ability of the simian prototypes of our vaccines to induce immune responses that can prevent infection as well as reduce the levels of viral replication in those animals that become infected.

Encouragingly, we found that non-human primates that were protected against a first series of rectal challenges were protected against further series of challenges. Seven survivors from a first series of 12 exposures were rested a year, boosted once with the MVA vaccine, and then exposed to a 2nd series of challenges. One of 7 animals was infected by the 10th exposure. Survivors of this 2nd series of exposures were again rested for 6 months and then exposed to a 3rd series of challenges. Again, protection was seen against the challenges with the last animal not becoming infected until the 12th challenge. The 1st two series of exposures were to SIVE660, a virus that has neutralization characteristics like viruses undergoing transmission in the current epidemic. The 3rd series of challenges was with SIV251, a virus that is considered the most potent SIV used in nonhuman primate studies and is an outlier in its high resistance to neutralization. 

Completed Human Clinical Trials -- Preventive HIV Vaccine

Preclinical Studies – Therapeutic Vaccine. In 2007-2008, data were generated in three pilot studies on therapeutic vaccination in simian immunodeficiency virus-infected non-human primates. The vaccine used in these pilot studies was specific for simian immunodeficiency virus but with the design features of our HIV/AIDS vaccine. In these pilot studies, conducted at Yerkes National Primate Research Center of Emory University, non-human primates were infected, drug-treated, vaccinated and then drug-interrupted. Following treatment interruption, median levels of virus in blood, measured as viral RNA, were 10 to 1000-times lower than those measured prior to drug and vaccine treatment. The therapeutic reductions in virus levels were best for animals placed on within 12 weeks of infection with lower levels of protection being achieved in animals that were placed on drugs at 3 months or later after infection.

Preventive Vaccine — Phase 1 Human Clinical Trials.All of our preventive vaccination trials in humans have been conducted by the HVTN, a network that is funded and supported by the NIH. The HVTN is the largest worldwide clinical trials network focused on the development and testing of HIV/AIDS vaccines. The results of a two group, 30 participant, Phase 1 trial (designated HVTN 045) are published inAIDS RESEARCH AND HUMAN RETROVIRUSES22:678 (2006) and of a four group 120 participant trial (HVTN 065) inThe Journal of Infectious Diseases 203:610 (2011). Our Phase 1 trials have tested both safety and dosing regimens.

InIn our first Phase 1 clinical trial, HVTN 045, our DNA vaccine was tested without MVA boosting to document the safety of the DNA. Our second Phase 1 clinical trial, HVTN 065, was designed to test the combined use of DNA and MVA and consisted of a dose escalation as well as regimen studies. The low dose consisted of 0.3 mg of DNA and 1x1071x10⁷ tissue culture infectious doses (TCID50) of MVA. Once safety was demonstrated for the low dose in 10 participants, the full dose (3 mg of DNA and 1x1081x10⁸ TCID50 of MVA) was administered to 30 participants. A single dose of DNA at time 0 followed by MVA at weeks 8 and 24, a DMM regimen, and three doses of MVA administered at weeks 0, 8 and 24, an MMM regimen, were also tested in 30 participants each. Participants were followed for 12 months to assess vaccine safety and to measure vaccine-induced immune responses.

Data from the HVTN 065 trial again documented the safety of the vaccine products but also showed that the DDMM and MMM regimens induced different patterns of immune responses. The full dose DDMM regimen induced higher response rates of CD4++ T-cells (77%) and CD8++ T-cells (42%) compared to the MMM regimen (43% CD4CD4+ and 17% CD8CD8+ response rates). In contrast, the highest response rates and highest titers of antibodies to the HIV Env protein were induced in the group that received only the MVA using the MMM regimen. Antibody response rates were documented to be higher for the MMM group using three different assays designed to measure total binding antibody levels for an immune dominant portion of the Env protein (27% for DDMM and 75% for MMM), binding of antibodies to the gp120 subunit of the envelope glycoprotein (81% for DDMM and 86% for MMM) and neutralizing antibodies (7% for DDMM and 30% for MMM). The 1/10th dose DDMM regimen induced overall similar T-cell responses but reduced antibody responses while the response rates were intermediate in the DMM group.

The HVTN also sponsored and conducted a Phase 1 clinical testingtrial in humans (HVTN 094) of the adjuvanted form of our vaccine that co-expresses GM-CSF in the DNA priming vaccine. This adjuvantedWe have designated the GM-CSF-adjuvanted version of our DNA/MVA vaccine regimen as GOVX-B21, and the unadjuvanted version as GOVX-B11. During December 2013, we reviewed preliminary results from HVTN 094. Based on excellent preclinical non-human primate data, this trial was originally initiated with the expectation that GOVX-B21 would be carried forward into Phase 2 testing by the HVTN, with support by the NIH. However, comparison of data between HVTN 094 and the Phase 2a trial, HVTN 205 (see below) did not elicit superior immune responsesshow a significant benefit from adding the adjuvant to the unadjuvanted vaccine and isfor preventive use; therefore GOVX-B21 was not being further advanced in preventive trials.further clinical testing (results to be published).

Preventive Vaccine — Phase 2 Human Clinical Trials.Based on the safety and the immunogenicity results in the HVTN 045 and HVTN 065 trials, the full dose DNA/MVA and MVA-only regimens of our first-generation vaccine were selected for testing by the HVTN in a Phase 2a trial (designated HVTN 205) which was completed in 2012 and the subject of an oral presentation at theAIDS Vaccine 2012 Conference in September 2012, with further analysis presented at theAIDS Vaccine Meeting in Barcelona, Spain, in October 2013.2013 and a publication in theJournal of Infectious Diseases (volume 210, pg 99)in 2014. HVTN 205 was designed to evaluate the safety and immunogenicity of our vaccines in healthy, HIV-uninfected adults. In HVTN 205, 299 participants were randomly assigned to three study arms: 149 participants received two injections of our DNA vaccine followed by two injections of the our MVA vaccine (DDMM arm), 75 participants received three MVA injections followed byand one placebo injection (MMM(MMPM arm), and 75 participants received four injections of placebo. After the final vaccination, antibody responses against the HIV Envelope protein (Env), the target for protective antibody, were detected in 93.2% of the DDMM arm (the vaccination regimen selected for further clinical study). At six months after final vaccination (the latest time point tested), Gp140gp140 IgG antibody response titers in the DDMM arm had declined by less than 3-fold, with response rates only declining from 100% to 84%, indicating significant durability of the antibody response. Additionally, HVTN 205 also showed that the antibody responses after vaccination had high affinity binding, a characteristic which has been associated with prevention of HIV infection in preclinical models. The study also showed low response rates for serum IgA, a desirable characteristic because serum IgA competed with serum IgG for reducing the risk of infection in the one partially protective (31%) AIDS vaccine trial in Thailand. Response rates for serum IgG3, an isotype associated with activating innate methods of protection such as complement (C’)-mediated lysis and antibody-dependent cellular cytotoxicity were excellent (91%).

Phase 2b Trial Planning.HIV Immunotherapy ProgramCurrently we are in discussion with the HVTN on moving the unadjuvanted vaccine into Phase 2b efficacy testing in the Americas.

Therapeutic Vaccine —Human Clinical Trials.To help treat those people whoCurrent antiretroviral therapies, though highly effective at suppressing HIV viral load, are already infected withunable to eliminate HIV we are testinginfection entirely. A major challenge in the feasibilitydevelopment of using our vaccineHIV therapeutics is the ability of HIV to enhance viral controlpersist in drug-treated individuals. Antiretroviral therapeutic drugs,host cells in a latent proviral form, invisible to the immune system and inaccessible to antiretroviral drugs. In response to this problem, the NIH and other leaders in the HIV field have developed a new concept: the “shock and kill” strategy, in which are taken for life by individuals once infected withpatients remain on standard-of-care anti-retroviral drug therapy while a second drug (“shock agent”) is used to activate latent HIV have side effects and are expensive, costing $12,000 - $15,000 per year (drug cost only, not including physician visitsa third drug (“kill agent”) is used to recognize and related costs). And accordingeliminate cells that harbor the latent HIV reservoir. A shock and kill therapy could potentially contribute to a 2010 study bycure for HIV.

Observations from a pilot Phase 1 clinical trial of our HIV vaccines (GV-TH-01 – discussed below) have led us to postulate that our DNA vaccines may be effective as a shock agent and that a subsequent, precisely timed MVA inoculation may reduce viral reservoirs. The Company is currently considering the CDC,best course of action for advancing its HIV immunotherapy program. Future therapeutic studies of GeoVax’s vaccine may investigate vaccine’s ability to act as a “shock agent” in a shock and kill therapy in combination with standard of care antiretroviral drug therapy to seek a cure. The timetable and specific clinical plans will be dependent upon the Company’s ability to secure external funding for the program, and on the nature of any potential collaborations GeoVax may establish.

Preclinical Studies – Therapeutic Vaccine. In 2007-2008, data were generated in three pilot studies on therapeutic vaccination in simian immunodeficiency virus-infected non-human primates. The vaccine used in these pilot studies was specific for simian immunodeficiency virus but with the design features of our HIV/AIDS vaccine. In these pilot studies, conducted at Yerkes National Primate Research Center of Emory University, non-human primates were infected, drug-treated, vaccinated and then drug-interrupted. Following treatment interruption, median levels of virus in blood, measured as viral RNA, were 10 to 1000-times lower than those individualsmeasured prior to drug and vaccine treatment. The therapeutic reductions in the United States who are diagnosedvirus levels were best for animals placed on drugs within 12 weeks of infection with HIV, only 35% ultimately achieve stable viral load suppression through drug treatment.  Thus, evenlower levels of protection being achieved in the United States where the availability ofanimals that were placed on drugs and treatment is good, there is still obvious compelling need for therapies that complement drugs.at 3 months or later after infection.

Phase 1 Trial (Treatment Interruption). We are conductingIn early 2014, we completed a Phase 1 clinical trial (GV-TH-01) investigating the therapeutic use of our vaccines in HIV-infected individualspatients. GV-TH-01 is an open label Phase 1 treatment interruption trial investigating the safety and immunogenicity of our DNA/MVA vaccine regimen in 9 HIV-infected patients who began successful antiretroviralinitiated drug treatment within 18 months of seroconversion and had stably controlled virus for at least 6 months. Patients were vaccinated with two DNA inoculations followed by two MVA inoculations at intervals of two months. Eight weeks following the last inoculation, patients suspended drug therapy for a negative HIV-1 antibody test.12-week period. Vaccinated patients’ ability to control the time and temporal height of re-emergent virus in the absence of drugs was then observed. Drug treatment was re-instituted after 12 weeks, and trial participants were observed for an additional 6 months. The primary goalsendpoint of this clinical trial arestudy was to documentevaluate the safety and immunogenicity of theour vaccine in HIV-positive patients with well-controlled infections.infections who are being treated with oral HIV medications. An exploratory objective isof the study was to assessevaluate the ability of the vaccinevaccinated patient to control re-emergent virus during a 12 week period ofthe drug treatment interruption. We are near completion of this 9 participant study and will be presenting findings at CROI in March of 2014.interruption period.

Phase 1 Trial Planning (Vaccine plus StandardAnalysis of Care Drug Therapy). The NIH has recently prioritized searching for a cure for those individuals who are HIV positive. BecauseGV-TH-01 data indicates that, during the vaccination phase of the mechanisms by which current oral drugs work, iftrial, enhanced CD8++ T cells were elicited in 8 of 9 participants and enhanced CD4++ T cell in 5 of 9 participants. Antibody responses were boosted in 4 of 9 participants. Analyses during the virus is in a latenttreatment interruption phase these drugs are not effective, thus the drugs can prevent spread of the virus but cannot kill an infected cell. Immunetrial suggested that individuals with the best immune responses can recognizehad lower levels of re-emergent virus. These levels however were not sufficiently low to prevent immune escape and kill infected cells if they are expressing viral protein. We are currently developing a protocolthe reinstitution of progression towards AIDS. Excellent safety was observed throughout the trial, with none of the participants needing to reinstate antiretroviral drugs during the treatment interruption phase of the trial (data being compiled for testing vaccination in the presence of continuous drug treatment to test whether we can reduce viral reservoirs by combining our vaccine with drugs. We will be submitting a grant proposal to fund this study which, if accepted, would allow a start date in early 2015.publication).

Support from the United States Government

With the exception of the GV-TH-01 Phase 1 therapeutic trial (treatment interruption protocol), all of our human clinical trials to date have been conducted by the HVTN and funded by NIH. This financial support has been provided by the NIH directly to the HVTN, so has not been recognized in our financial statements. Our responsibility for these clinical trials has been to provide sufficient supplies of vaccine materials and technical expertise when necessary.

In addition to clinical trial support from the NIH, our operations arehave been partially funded by NIH research grants. In September 2007, the NIH awarded us an Integrated Preclinical/Clinical AIDS Vaccine Development (IPCAVD) grant to support our HIV/AIDS vaccine program. We are utilizing this funding to further our HIV/AIDS vaccine development, optimization and production. The aggregate award (including subsequent amendments) totaled $20.4 million, and there is approximately $773,000 remaining and available for use as of September 30, 2013. In September 2012, the NIH awarded us an additional grant of $1.9 million to support development of versions of our HIV/AIDS vaccines to address the clade C subtype of the HIV virus prevalent in the developing world. All funding pursuant to this grant has been utilized. In July 2013, the NIH awarded us a Small Business Innovative Research (SBIR) grant for approximately $277,000 to support preclinical studies evaluating the ability of protein boosts to augment antibody responses. The grant award of approximately $277,000 is for the first year of a two year project period beginning August 1, 2013, with a total award of approximately $566,000.

Please referRefer to our Financial Statements beginning on page F-1 of this prospectus,Prospectus, and to “Management's Discussion and Analysis of Financial Condition and Results of Operations”, for additional information regarding revenue.revenue and funds availability from these grants.

Regulations

Regulation by governmental authorities in the United States and other countries is a significant factor in our ongoing research and development activities and in the manufacture of our products under development. Complying with these regulations involves a considerable amount of time and expense.

In the United States, drugs are subject to rigorous federal and state regulation. TheOur products are regulated under the Federal Food, Drug and Cosmetic Act, as amended or the FDC Act,(FD&C Act), and the regulations promulgated thereunder, and other federal and state statutes and regulationsregulations. These laws govern, among other things, the testing, manufacture, safety, efficacy, labeling, storage, record keeping, approval, advertising and promotion of medications and medical devices. Product development and approval within this regulatory framework is difficult to predict, takes a number of years and involves great expense. The steps required before a pharmaceutical agenthuman vaccine may be marketed in the United States include:

Each of these steps is described further below. Before marketing any drug or biologic for human use, the product sponsor must obtain FDA approval. In addition, to obtaining FDA approval for each product, each domestic manufacturing establishment must be registered with the FDA and approved by,must pass a Pre-Approval Inspection (PAI) before introducing any new drug or biological product into commercial distribution. Because GeoVax does not manufacture vaccines for human use within our own facilities, we must ensure compliance both in our own operations and in the FDA. Domesticoutsourced manufacturing operations. All FDA-regulated manufacturing establishments (both domestic establishments and foreign establishments that export products to the United States) are subject to biennial inspections by the FDA and must comply with the FDA’s Good Manufacturing Practices for products, drugs and devices.

FDA determines compliance with applicable statutes and regulations through documentation review, investigations, and inspections. Several enforcement mechanisms are available to FDA, ranging from a simple demand to correct a minor deficiency to mandatory recalls, closure of facilities, and even criminal charges for the most serious violations.

Preclinical Testing.Pre-clinicalPreclinical testing includes laboratory evaluation of chemistry and formulation, as well as cell culture and animal studies to assess the safety and potential efficacy of the product. Pre-clinicalPreclinical safety tests and certain other pivotal preclinical studies must be conducted by laboratories that comply with the FDA’s Good Laboratory Practices, or GLP. The results of pre-clinical testing are submitted to the FDA as part of the IND application and are reviewed by the FDA prior to the commencement of human clinical trials. Unless the FDA objects to an IND, the IND becomes effective 30 days following its receipt by the FDA.

cGMP-Compliant Manufacturing and Testing.FDA has issued, and frequently updates, extensive regulations on current Good Manufacturing Practice (cGMP). Any drug, biologic, or device for human use, whether commercial or investigational, must be manufactured under these regulations. cGMP regulations include a wide variety of requirements covering personnel, documentation, facilities, equipment, testing procedures, and many other aspects of manufacturing and testing.

Clinical Trials.Clinical trials involve the administration of the HIV vaccinesinvestigational drugs to volunteers or to patients under the supervision of a qualified, medically trained principalclinical investigator. Clinical trials are conducted in accordance with Good Clinical Practices under protocols that detail the objectives of the trial, the parameters to be used to monitor safety and the efficacy criteria to be evaluated. Each protocol and the qualifications of the investigators who plan to carry it out must be submitted to the FDA as part of the IND. Further, each clinical trial must be conducted under the auspices of an independent institutional review board at the institution where the trial will be conducted. The institutional review board will consider, among other things, ethical factors, the safety of human subjects and the possible liability of the institution.

Clinical trials are typically conducted in three sequential phases, but the phases may overlap. In the Phase 1 clinical trial, the initial introduction of the product into healthy human subjects, the vaccine is tested for safety (including adverse side effects) and dosage tolerance. The Phase 2 clinical trial is the proof of principal stage and involves trials in a limited patient population to determine whether the product induces the desired effect (for our vaccines this means immune responses) and to better determine optimal dosage. The continued identification of possible safety risks is also a focus. When there is evidence that the product may be effective and has an acceptable safety profile in Phase 2 clinical trials, Phase 3 clinical trials are undertaken to evaluate clinical efficacy and to test for safety within an expanded patient population. Phase 3 trials are completed using multiple clinical study sites which are geographically dispersed. The manufacturer or the FDA may suspend clinical trials at any time if either believes that the individuals participating in the trials are being exposed to unacceptable health risks.

New DrugBiologics License Application and FDA Approval Process.The results and details of the pre-clinical studies and clinical trials are submitted to the FDA in the form of a New Drug Application. IfBiologics License Application (BLA), which is equivalent to the New Drug Application (NDA) submitted by companies seeking to market new drugs. If the BLA is approved, the manufacturer may market the product in the United States. Under the Prescription Drug User Fee Act (PDUFA), FDA charges user fees to applicants to offset the costs of its operations. The PDUFA user fee for a new vaccine is over $2 million, unless the applicant obtains a waiver or reduction through certain programs designed to encourage development of certain types of products.

Postmarketing Requirements. FDA frequently imposes postmarketing requirements as a condition of NDA or BLA approval. Common postmarketing requirements include additional clinical trials (Phase 4 trials) or observational studies. Postmarketing requirements are especially relevant to our Ebola and Marburg vaccines. We intend to pursue approval of these vaccines using the accelerated approval process, in which FDA grants approval based on performance against a criterion other than actual protection against the disease but requires the manufacturer to monitor and submit data on efficacy of the approved product. Unlike pathogens such as human papillomavirus, Ebola and Marburg are not constantly in circulation; instead, they occur in sporadic but extremely deadly outbreaks. For this reason, it would be impractical and potentially unethical to attempt to perform a traditional Phase 3 trial in which vaccinated participants are compared against unvaccinated participants to determine the efficacy of the vaccine in preventing infection with Ebola or Marburg. The accelerated approval process allows FDA to approve a new medicine based on its performance against a surrogate endpoint (in the case of Ebola or Marburg, its performance in raising immune responses). We anticipate that, as a condition of receiving accelerated approval, GeoVax would agree to monitor the real-world performance of our Ebola and Marburg vaccines.

International Approval.Whether or not the FDA has approved the drug, approval of a product by regulatory authorities in foreign countries must be obtained prior to the commencement of commercial sales of the drug in such countries. The requirements governing the conduct of clinical trials and drug approvals vary widely from country to country, and the time required for approval may be longer or shorter than that required for FDA approval.

Other Regulations.In addition to FDA regulations, our business activities may also be regulated by the Occupational Safety and Health Act, the Environmental Protection Act, the Toxic Substances Control Act, the Resource Conservation and Recovery Act and other present and potential future federal, state or local regulations. Violations of regulatory requirements at any stage may result in various adverse consequences, including regulatory delay in approving or refusal to approve a product, enforcement actions, including withdrawal of approval, labeling restrictions, seizure of products, fines, injunctions and/or civil or criminal penalties. Any product that we develop must receive all relevant regulatory approvals or clearances before it may be marketed.

Manufacturing

We do not have the facilities or expertise to manufacture any of the clinical or commercial supplies of any of our products. To be successful, our products must be manufactured in commercial quantities in compliance with regulatory requirements and at an acceptable cost. To date, we have not commercialized any products, nor have we demonstrated that we can manufacture commercial quantities of our product candidates in accordance with regulatory requirements. If we cannot manufacture products in suitable quantities and in accordance with regulatory standards, either on our own or through contracts with third parties, it may delay clinical trials, regulatory approvals and marketing efforts for such products. Such delays could adversely affect our competitive position and our chances of achieving profitability. We cannot be sure that we can manufacture, either on our own or through contracts with third parties, such products at a cost or in quantities whichthat are commercially viable.

We currently rely and intend to continue to rely on third-party contract manufacturers to produce vaccines needed for research and clinical trials. We have entered into arrangements with third party manufacturers for the supply of our DNA and MVA vaccines for use in our planned clinical trials. These suppliers operate under the FDA’s Good Manufacturing Practices and (in the case of European manufacturers) similar regulations of the European Medicines Agency. We anticipate that these suppliers will be able to provide sufficient vaccine supplies to complete our currently planned clinical trials. Various contractors are generally available in the United States and Europe for manufacture of vaccines for clinical trial evaluation, however, it may be difficult to replace existing contractors for certain manufacturing and testing activities and costs for contracted services may increase substantially if we switch to other contractors.

Development of Improved Manufacturing Techniques for MVA –The MVA component of our vaccine is currently manufactured in cells that are cultured from embryonated chicken eggs. Thiseggs, which is cumbersome and pronea reliable method to contamination during the processing of the eggs required to make amanufacture large batchquantities of vaccine. GeoVax hasIn an attempt to find a means to reduce costs for large-scale manufacturing, we have explored a number of approaches to growingproducing MVA in continuous cell lines that can be grown in bioreactors. In this process we have identified a duck stem-cell-derived line (termed EB66), that is proprietary to Valneva S.E., France. We are currently working with Valneva on the use of EB66 cells for the growth of our MVA vaccines andvaccines. We are pleased with the results the collaboration is obtaining. We anticipatehopeful that by the timeupon completion of this alternative process development is complete we will behave the option of producing vaccine at significantly higher titers in a much more advanced and scalable process, allowing for quality improvements over the current process as well as meaningful cost reductions. The U.S. FDA has reviewed our early-stage plans for transitioning from MVA growth in egg-derived cells to a continuous cell line.

Competition

There currently is no FDA licensed and commercialized HIV/AIDS vaccine or competitive vaccine available in the world market. However, the market for vaccines that protect against or treat HIV/AIDS is intensely competitive and is subject to rapid and significant technological change. We will have numerous competitors in the United States and abroad, including large companies with substantially greater resources than us. These competitors may develop technologies and products that are more effective or less costly than any of our future technology or products or that could render our technology or products obsolete or noncompetitive.

There are several small and largeThe biopharmaceutical companies pursuing HIV/AIDS vaccine research and development, including Novartis, Sanofi-Aventis and GlaxoSmithKline. Other HIV/AIDS vaccines are in varying stages of research, testing and clinical trials including those supported by the NIH Vaccine Research Center, the U.S. Military, IAVI, the European Vaccine Initiative,industry and the South African AIDS Vaccine Initiative.

In October 2009, the results from a Phase 3 community-based clinical trial in Thailand using a recombinant canarypox (designated ALVAC and produced by Sanofi Pasteur) as a priming vaccine and a bivalent mixture of the gp120 subunit of Env from HIV clades B and C (produced by VaxGen, Inc. and currently licensed to Global Solutions for Infectious Diseases) as a protein booster vaccine were reported. In this clinical trial, protection against HIV infection at the rate of 31% was reported. The results of this clinical trial are encouraging because they represent the first success of an AIDS vaccine in humans and demonstrate that a vaccine can provide protection against HIV infections. 

To our knowledge, none of our competitors’ products have been tested in large scale non-human primate trials that have included experimental infection through the rectal site and shown to induce levels of protection or duration of protection comparable to that achieved using experimental prototypes of GeoVax’s vaccines. Furthermore, many of our competitors’ vaccine development programs require vaccine compositions which are more complicated than ours. For these reasons, we believe that it may be possible for our vaccine to compete successfully in the marketplace if licensed.

Overall, the biopharmaceutical industrymarket is competitive and subject to rapid and substantial technological change. Developments by others may render our proposed vaccination technologies noncompetitive or obsolete, or we may be unable to keep pace with technological developments or other market factors. Technological competition in the industry from pharmaceutical and biotechnology companies, universities, governmental entities and others diversifying into the field is intense and is expected to increase. Many of the pharmaceutical companies that compete with us have significantly greater research and development capabilities than we have, as well as substantially more marketing, manufacturing, and financial resources. In addition, acquisitions of, or investments in, small pharmaceutical or biotechnology companies by such large corporations could increase their research, financial, marketing, manufacturing and other resources. Competitive technologies may ultimately prove to be safer, more effective or less costly than any vaccine that we develop.

There are currently no FDA licensed and commercialized Ebola vaccines, Marburg vaccines, or HIV vaccines available in the world market. We are aware of several development-stage and established enterprises, including major pharmaceutical and biotechnology firms, which are actively engaged in vaccine research and development in these areas. For Ebola, these include Johnson & Johnson, GlaxoSmithKline, and Merck. For HIV, these include Novartis, Sanofi-Aventis and GlaxoSmithKline. Other HIV vaccines are in varying stages of research, testing and clinical trials including those supported by the NIH Vaccine Research Center, the U.S. Military, IAVI, the European Vaccine Initiative, and the South African AIDS Vaccine Initiative. We may also experience competition from companies that have acquired or may acquire technologies from companies, universities and other research institutions. As these companies develop their technologies, they may develop proprietary technologies which may materially and adversely affect our business.

If any of our competitors develop products with efficacy or safety profiles significantly better than our products, we may not be able to commercialize our products, and sales of any of our commercialized products could be harmed. Some of our competitors and potential competitors have substantially greater product development capabilities and financial, scientific, marketing and human resources than we do. Competitors may develop products earlier, obtain FDA approvals for products more rapidly, or develop products that are more effective than those under development by us. We will seek to expand our technological capabilities to remain competitive; however, research and development by others may render our technologies or products obsolete or noncompetitive, or result in treatments or cures superior to ours.

FDAOur competitive position will be affected by the disease indications addressed by our product candidates and other regulatory approvalsthose of our vaccines have not yet been obtainedcompetitors, the timing of market introduction for these products and we have not yet generated any revenues from product sales. Our future competitive position dependsthe stage of development of other technologies to address these disease indications. For us and our competitors, proprietary technologies, the ability to complete clinical trials on oura timely basis and with the desired results, and the ability to obtain FDA and othertimely regulatory approvals to market these product candidates are likely to be significant competitive factors. Other important competitive factors will include the efficacy, safety, ease of our vaccinesuse, reliability, availability and price of products and the ability to license or sellfund operations during the vaccines to third parties on favorable terms.period between technological conception and commercial sales.

Our Intellectual Property

We will be able to protect our proprietary rights from unauthorized use by third parties only to the extent that our proprietary rights are described by valid and enforceable patents or are effectively maintained as trade secrets. Accordingly, we are pursuing and will continue to pursue patent protection for our proprietary technologies obtained or developed through our collaborations with Emory University, the NIH, and the CDC, or developed by us alone. Patent applications have been filed with the U.S. Patent and Trademark Office and in specific international markets (countries). Patent applications include provisionsOur patent portfolio, described more fully below, includes claims directed to cover our DNA and MVA based HIV vaccines, their genetic inserts expressing multiple HIV protein components, composition, structure, claim of immunization against multiple subtypes of HIV, routes of administration, safety and other related factors. Patent claims filed for our vaccines include provisions for theirfactors and methods of therapeutic and prophylactic use thereof including administration regimes. Also included are claims directed to preventive vaccines against HIVEbola and smallpox.Marburg viruses and use thereof. As of January 1, 2015, we are the licensee of at least eight issued or allowed U.S. patents and at least 12 issued or allowed non-U.S. patents. We are actively pursuing one U.S. provisional application and one international patent application as the owner of record, in addition to at least six U.S. patent applications and at least 15 non-U.S. patent applications in six jurisdictions under license.

We are the exclusive, worldwide licensee of a number of patents and patent applications, which we refer to as the Emory Technology, owned, licensed or otherwise controlled by Emory University for HIV or smallpox vaccines pursuant to a License Agreement originally entered into on August 23, 2002 and restated on June 23, 2004, which we refer to as the Emory License. Through the Emory License we are also a non-exclusive licensee of four issued United States patents owned by the NIH related to the ability of our MVA vector vaccine to operate as a vehicle to deliver HIV virus antigens, and also to induce an immune response in humans. The four issued United States patents owned by the NIH expire in 2023. All of our obligations with respect to the HIV NIH-owned MVA patents are covered by the Emory License. In addition to the issued United States patents owned by the NIH, and a recently issued patent owned by Emory University, there are six issued and seven pending United States patent applications, and thirty-two issued or pending patents in countries other than the United States. The Emory License expires on the expiration date of the last to expire of the patents licensed thereunder including those that are issued on patents currently pending. We will not know the final termination date of the Emory License until such patents are issued. The Company may terminate the Emory University License upon 90 days’ written notice. The Emory License also contains standard provisions allowing Emory University to terminate upon breach of contract by the Company or upon the Company’s bankruptcy.

The Emory License, among other contractual obligations, requires payments based on the following:

We may only use the Emory Technology for therapeutic or prophylactic HIV or smallpox vaccines. Emory University also reserved the right to use the Emory Technology for research, educational and non-commercial clinical purposes. Due to the use of federal funds in the development of the Emory Technology, the U.S. Government has the irrevocable, royalty-free, paid-up right to practice and have practiced certain patents throughout the world, should it choose to exercise such rights.

We are not a party to any litigation, opposition, interference, or other potentially adverse proceeding with regard to our patent positions. However, if we become involved in litigation, interference proceedings, oppositions or other intellectual property proceedings, for example as a result of an alleged infringement or a third-party alleging an earlier date of invention, we may have to spend significant amounts of money and time and, in the event of an adverse ruling, we could be subject to liability for damages, invalidation of our intellectual property and injunctive relief that could prevent us from using technologies or developing products, any of which could have a significant adverse effect on our business, financial conditions or results of operations. In addition, any claims relating to the infringement of third-party proprietary rights, or earlier date of invention, even if not meritorious, could result in costly litigation, lengthy governmental proceedings, divert management’s attention and resources and require us to enter royalty or license agreements which are not advantageous if available at all.

We are also the exclusive licensee of five patents from MFD, Inc., which we refer to as the MFD Patents, pursuant to a license agreement dated December 26, 2004 with MFD, Inc., which we refer to as the MFD license agreement, related to certain manufacturing processes used in the production of our vaccines. Pursuant to the MFD license agreement, we obtained a fully paid, worldwide, irrevocable, exclusive license in and to the MFD Patents to use, market, offer for sale, sell, lease and import any AIDS and smallpox vaccine made with GeoVax Technology, as such term is defined in the MFD license agreement, and non-exclusive rights for other products. The term of the MFD license agreement ends on the expiration date of the last to expire of the MFD Patents, one of which expires in 2017. The license granted also extends to any and all current or future customers of GeoVax the right to commercially practice the GeoVax Technology, as such term is defined in the MFD license agreement, or any portion thereof. The license also extends to any and all current or future GeoVax Users, as such term is defined in the MFD license agreement, the right to use any GeoVax Technology, as such term is defined in the MFD license agreement.

In addition to patent protection, we also attempt to protect our proprietary products, processes and other information by relying on trade secrets and non-disclosure agreements with our employees, consultants and certain other persons who have access to such products, processes and information. Under these agreements, all inventions conceived by employees are our exclusive property. Nevertheless, there can be no assurance that these agreements will afford significant protection against misappropriation or unauthorized disclosure of our trade secrets and confidential information.

We cannot be certain that any of the current pending patent applications we have licensed, or any new patent applications we may file or license, will ever be issued in the United States or any other country. Even if issued, there can be no assurance that those patents will be sufficiently broad to prevent others from using our products or processes. Furthermore, our patents, as well as those we have licensed or may license in the future, may be held invalid or unenforceable by a court, or third parties could obtain patents that we would need to either license or to design around, which we may be unable to do. Current and future competitors may have licensed or filed patent applications or received patents, and may acquire additional patents or proprietary rights relating to products or processes competitive to ours. In addition, any claims relating to the infringement of third-party proprietary rights, or earlier date of invention, even if not meritorious, could result in costly litigation, lengthy governmental proceedings, divert management’s attention and resources and require us to enter royalty or license agreements which are not advantageous to us, if available at all.

Research and Development

Our expenditures for research and development activities were $3,043,522, $4,276,375,$1,812,969, $2,914,878, and $4,793,956$3,043,522 during the years ended December 31, 2014, 2013 and 2012, 2011respectively; and 2010, respectively,$1,166,803 and $2,314,291$1,344,560 for the nine month period endingperiods ended September 30, 2013.2015 and 2014, respectively. As our vaccines continue to go through the process to obtain regulatory approval, we expect our research and development costs to continue to increase significantly as even larger human clinical trials proceed in the United States and foreign countries.proceed. We have not yet formulated any plans for marketing and sales of any vaccine candidate we may successfully develop. Compliance with environmental protection laws and regulations has not had a material effect on our capital expenditures, earnings or competitive position to date.

Properties and Employees

We lease approximately 8,400 square feet of office and laboratory space located at 1900 Lake Park Drive, Suite 380, Smyrna, Georgia under a 62 month lease agreement which began November 1, 2009.2009, with an original expiration date of December 31, 2014. We have renewed the lease through December 31, 2016, with a 12-month renewal option. We believe this space is adequate for our current needs. As of December 31, 2013,8, 2015, we had eightsix full-time and three part-time employees. None of our employees are covered by collective bargaining agreements and we believe that our employee relations are good.

CorporateCorporate Background

Our primary business is conducted by our subsidiary, GeoVax, Inc., which was incorporated under the laws of Georgia in June 2001. The predecessor of our parent company, GeoVax Labs, Inc. (the reporting entity) was originally incorporated in June 1988 under the laws of Illinois as Dauphin Technology, Inc. (“Dauphin”). In September 2006, Dauphin completed a merger (the “Merger”) with GeoVax, Inc. As a result of the Merger,merger, GeoVax, Inc. became a wholly-owned subsidiary of Dauphin, and Dauphin changed its name to GeoVax Labs, Inc. In June 2008, the Company was reincorporated under the laws of Delaware. We currently do not conduct any business other than GeoVax, Inc.’s business of developing new products for the treatment or prevention of human diseases. Our principal offices are located in Smyrna, Georgia (metropolitan Atlanta).

AVAILABLE INFORMATION

Our website address is www.geovax.com. We make available on this website under “Investors – SEC Reports,” free of charge, our proxy statements, annual reports on Form 10-K, quarterly reports on Form 10-Q, current reports on Form 8-K and amendments to those reports as soon as reasonably practicable after we electronically file or furnish such materials to the SEC. We also make available our Code of Ethics on this website under the heading “Investors – Corporate Governance”. Information contained on our website is not incorporated into this prospectus.

SELECTED FINANCIAL DATA

The following selected financial data as of and for each of the five years ended December 31, 2014 are derived from our audited and unaudited consolidated financial statements. The selected financial data as of and for the nine months ended September 30, 2015 and 2014 is unaudited. The historical results presented below are not necessarily indicative of the results to be expected for any future period. The information set forth below should be read in conjunction with the information contained in “Management’s Discussion and Analysis of Financial Condition and Results of Operations”, and our consolidated financial statements and the related notes, beginning on page F-1 of this prospectus. Our historical results are not necessarily indicative of the results to be expected for any future periods.