BioClonetics Immunotherapeutics: Designing the first cure for HIV through the use of monoclonal antibodies

Tomasz Zastawny, DSc, Ph.D.

Chief Clinical Operations Office

Drug Development Executive with 20 years of global, cross-functional experience in Clinical Research, CMC, QA, Regulatory Affairs and Project Management in various therapeutic areas.

Paul D. Fellegy

Chief Financial Officer

Over 25 years of experience in the financial field working with national financial groups in a variety of roles.

Gaurav Chandra

COO & Vice President Research and Development

A qualified Healthcare Professional with 15 years of experience with demonstrated continuous growth, achievements, and impressive leadership within the healthcare industry.

Investor Q&A

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What does your company do?

BioClonetics is finalizing the production and testing of a monoclonal antibody to treat patients with HIV. HIV is a virus that infects 37 million and kills approximately 1.2 million every year, and today there is still no cure. At BioClonetics, we've created a cell line that produces fully human monoclonal antibodies to specifically target and neutralize infectious diseases including HIV. If successful, this could be the first true cure for HIV at a fraction of the price of current treatment.

Where will your company be in 5 years?

Despite claiming the lives of 400 children and 3000 adults every 24 hours, HIV has not received the public attention or private investment that it deserves. Many people think the HIV outbreak is over, but for millions of people worldwide it is still a terrifying reality. Today, 60% of those infected with HIV have no treatment while the 40% who are treated are treated using ARVs which are both toxic and expensive. BioClonetics is committed to finding an accessible and affordable HIV cure.

What is BioClonetics?

BioClonetics is a biotech company with a primary focus onfinalizing the production and testing of a monoclonal antibody to treat patientswith HIV. HIV is a virus that infects 37 million people and today there is nocure. Approximately 1.2 million individuals die from the virus each year. Thereis a lot of interest in monoclonal antibodies, and we have one that has beentested and proven to neutralize the virus. We are in the process of completingthe development of that monoclonal, testing it, and in the near future expectto make it available to patients.

What treatments are available for HIV today?

Treatment today is with a prescription for what are called antiretroviral drugs. The therapy is often referred to by the acronym ARV. ARVs suppress the virus, but do not cure. ARVs have some substantial shortcomings. They are known to cause severe damage to organs (including the heart and kidneys), decrease bone-mineral density, result in vitamin D insufficiency and must be administered for life. Other side effects may include hypersensitivity reactions, fat redistribution and immune reconstitution syndrome. ARVs are a lifelong treatment and their administration requires continual monitoring and adjustments in patient use. And over time, the antiretroviral drugs can become ineffective. The average lifelong cost for one patient’s antiretroviral therapy is currently $380,000. That's the lifetime cost per patient even though the health and physical condition of the patient can degrade over time as a result of the virus and use of these medications. Antiretrovirals are the only treatment option today, and while they can keepHIV-positive patients alive, they have the shortcomings mentioned. Additionally only 40% of those infected with HIV around the world have access to antiretroviral drugs because they are not available everywhere. Thus, over half of those infected with HIV have no therapy to keep them alive and healthy.

How are antibody treatments like yours different?

The human body is home to literally tens of thousands of antibodies, theoretically one for each of the many potential antigens (viruses, bacteria, toxins, etc.) that our bodies might be exposed to. Thus, antibodies are naturally produced in our bodies to control these harmful foreign invaders. When our bodies are exposed to one of these antigens, such as a virus, in most cases, the appropriate antibodies latch on to it and signal other components in the blood to remove the invader. In the case of HIV, the body initially produces antibodies to the virus when we are exposed. Unfortunately, the body's naturally formed antibodies are not able to control or remove the virus from our bodies - at least not for 98% of these infected with the virus. In other words, in 98% of the population that contract HIV, the antibodies produced by the body are not sufficient to control the virus, or neutralize it. That’s one of the interesting points about how our antibody was discovered. My brother, Dr. Joseph Cotropia, is a doctor who discovered the antibody. When the virus first came on the scene in the 1980's, he treated patients who had HIV. He recognized that some of his patients had the virus but did not become ill. What Dr. Cotropia did was take the white blood cells from a number of patients and isolate and then clone cell lines to produce specific antibodies that he could test. From the many that he produced, he found one antibody (now called Clone 3) that when tested against a full panel of HIV virus strains neutralized the virus. Fast forward to the current period. Of the people who contract the virus, 2% are what are called long-term non-progressors, they have an antibody, and expected they have the antibody we are developing, that is sufficient to control the virus. We have tested our antibody against multiple strains of the virus found around the world. The results of these tests have shown that the antibody does indeed neutralize or kill over 95% of the strains of virus against which it was tested. These tests were conducted in renown institutions including Univ. of California, San Francisco, CA, (Jay Levy, M.D.), Univ. of South Florida, Tampa, FL, (Kenneth Ugen, Ph.D.), Polymun Scientific, GmbH, Vienna, AUSTRIA, (Hermann Katinger, Ph.D.), Duke Univ., Durham, NC, (David Montefiori, Ph.D.) and Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, (Ruth Ruprecht, M.D., Ph.D.)

Is anyone else working on a similar treatment?

Researchers working on the virus in the beginning were, unfortunately, not working with patients in the normal day-to-day doctor-patient relationship. They were mostly treating patients who had the virus, were ill, and perhaps dying or near death. These patients likely did not have this particular antibody that was the secret to long-term non-progression.There are others testing monoclonal antibodies. We have discussed our findings with several multi-billion dollar U.S. pharma companies. One, for example, is developing an anti-HIV monoclonal antibody as well. But when you look at their monoclonal, and the tests results published, one finds that it faces what is called "virus escape". It's a way of saying the antibody attaches to the virus at a point that mutates. Which means it will not be effective in the real world. It works for a while and then the virus mutates to avoid any effectiveness.In contrast, our monoclonal attaches to the virus at a site that does not mutate - in other words, the Achilles heel of the virus exists in virtually all strains of the virus. Let me explain how we know this. There are over 4,000 currently known strains of the HIV virus. Imagine taking those 4,000 strains and putting their sequences of amino acid combinations into a computer so you know every location and every amino acid sequence in this long string of pearl amino acids that make up each virus strain. Let's assume you know where on the virus a particular antibody binds. Then you search all 4,000 strains and determine whether that Achilles' heel of the virus shows up in each one. Knowing exactly where our antibody attaches and by doing that search, we find that 98% of the 4,000 strains have the Achilles' heel to which our virus attaches.Other pharma antibodies bind to the virus at a different location. If one did a search of all 4,000 strains, the location of their attachment point would probably not appear in many of them. To be effective in the real world, you must have an antibody that binds to a location on the virus that exists in all or a very high percentage of the 4,000 strains.Another interesting fact is that as the database of these strains has been updated over the years, the Achilles' heel location to which our antibody binds continues to appear in 98% of all the newly identified HIV viruses. That means nature requires that every new strain maintain this location, probably for purposes of being able to replicate itself. This tells us that that the next 4,000 new strains that are found can be expected to also have this same Achilles' heel.

What prevents a competitor from getting the treatment approved first?

We are currently developing the recombinant of the Clone 3 antibody that will be the commercial product used in patient therapy. The now known sequence of therecombinant will be patentable in that we have identified the light chain andheavy chain amino acid sequences that program for the full recombinantmolecule. Such sequences are protectable through claims in patents, bothin the US and in foreign countries, to the exclusion of competitors. One step further will be the production and patenting of the mini-antibody sequences for treating HIV patients based on the knowledge known regarding Clone 3. This involves patent claims to small peptides selected from (1) blocking peptides that bind to the HIV-1 virus, thereby preventing the virus from binding to the target human CD4+ cell and (2) competitive peptides which bind to the surface of the target human CD4+ cells, whereby said binding prevents the virus from binding to the target CD4+ cell. Neutralization of the virus can be achieved by way of these two routes, either by an inhibitor binding directly to the virus thereby preventing the virus from binding to the target CD4+ cells, or by an inhibitor binding to the CD4+ cells, thereby preventing the virus from gaining access to the cell. As to this second method of preventing the virus from gaining access to the human cell, a compound would be created that “competes” with the virus’s attempt to bind to the human blood cell. Knowing where our antibody binds to the virus, we also know the know the location on the human blood cell to which the virus binds. Thus, our patent will claim competitive peptides which bind to the surface of the target human CD4+ cells, such binding preventing the virus from binding to the target human CD4+ cell. Both of these products will be patentable and will be a likely commercial use of our technology. Moreover, in our progress, the antibody will be made more potent through optimization and those improvements will be subject to patent protection. All of these patents will be important commercially by providing exclusivity to the company of our technology. Additionally, one must realize that no other company has the cell line that produces our monoclonal – thus reproduction our antibody will not be possible without this access.

What has your research found so far?

My brother, Dr. Joseph Cotropia, theorized at the outset that the best strategy was to attempt to isolate antibodies from white blood cells, called leukocytes, of HIV positive individuals who showed a natural resistance to the virus. He then tested the antibodies against strains of the HIV virus. One could only hope that the antibodies produced would be virus neutralizing. Once monoclonal antibodies were isolated, they were tested in five laboratories around the world. Those tests occurred over several years. The results of those tests showed that one of the antibodies, called Clone 3, neutralized (killed) 34 of the of the 39 strains tested. Where we are today is, the cell line that produces the Clone 3 antibody, as is normally the case, is a slow producer of the antibody. It would not produce enough medication to treat 36 million people. Therefore, we had to first identify the light chain and heavy chain sequence of the antibody to produce a substitute or recombinant cell line that is a “fast producer”. One way to imagine this is if you had a one perfect copy of a Michael Jackson audio recording, you’re not going to make a profit if you have only one copy so you must replicate it using a machine that could produce a million copies. To do that in an antibody, you have to sequence the light chain and heavy chain and produce the recombinant using a fast producing CHO cell line. In other words, you take the Michael Jackson audio record and you put it into a machine capable of producing a million copies. Once you produce the copies of Michael Jackson's vocal, you want to test it to see if it sounds the same. In the Michael Jackson case, you would present it to an audience. You might run it through some kind of analog device to see whether the sound was the same. That’s the stage we are at right now. We producing the antibody in a fast producing a CHO cell line followed by testing this newly produced recombinant antibody against various strains of the virus. These initial tests in the test tube are the equivalent to taking the Michael Jackson audio and playing it to an audience of 100 people. Once the first tests show effectiveness in test tube tests, then the antibody is tested it in macaque monkeys. This would be equivalent to testing Michael Jackson reproduced song by playing it to 1000 listeners. Once we have the same result in animal trials, then we move on to patient trials and then patient application. That's when you put the Michael Jackson record on the Internet for sales. That's where you make the greatest application of the technology, in the actual application for patients.

What are your expectations for FDA approval?

While there are no monoclonal antibodies approved today for treatment of HIV patients, monoclonal antibodies are the fastest growing segment of the pharmaceutical industry. They are at the forefront of therapeutic treatment of many diseases - such as rheumatoid arthritis, MS, Ebola and some forms of cancers. The acceptance of monoclonal antibodies in therapeutic treatment can be seen by the dramatic rise is sales of such antibodies - from $27 Billion in 2007 to $44 Billion in 2015. The expectation is that sales will increase 10% each year till 2020. The next step of preparing the antibodies in a CHO cell line is called recombinant preparation. We expect production of the recombinant to be completed in three to six months and testing against HIV isolates to be completed in eight months. The total cost of these 2 steps will be less than $300,000. Then animal trials can be completed in nine to twelve months. Animal trials will cost approximately $650,000 to $700,000. Thus, we project that we will complete animal trials in less than 24 months. Then we can move on to human trials.

What are your biggest worries moving forward?

In the next 3 steps in our development of our antibody, namely (1) creation of the recombinant of the Clone 3 antibody in a CHO cell line, (2) testing the recombinant against a full panel of HIV isolates and (3) conducting macaque animal, setbacks could naturally occur. However, all of the foreseen obstacles have possible solutions. Possible difficulties could arise in creating a stable permanent CHO cell line; the cell line might only secret non-neutralizing recombinant antibody; or the CHO cell line might not create a sufficient quality or quantity of antibody. Once the recombinant cell line is produced, the resultant antibody has to be confirmed to demonstrate the same effectiveness against HIV isolates tested as has the parent cell line produced monoclonal antibody. In the macaque trials, the results have to validate the neutralizing capability of the Clone 3 antibody previously demonstrated in test tube tests. However, potential deficiencies can be overcome. For example, one or more CHO cell line can readily be produced and there are known methods for increasing the potency of a monoclonal were one knows the light chain and heavy chain sequences – which we know. The important aspect of our monoclonal is that it targets (binds to) a site on the virus that does not mutate. Thus, we expect that it will be effective to provide an effective treatment for patients. In contrast, Pharma companies testing other anti-HIV monoclonals have found that they experience what is called “virus escape”, meaning the virus mutates around the antibody's effectiveness. In these cases, there is no way to improve effectiveness without identifying a wholly different antibody altogether.

How do you envision the product eventually making it to market?

After completion of animal trials and we approach human trials, there are ways to fast track a medication to treatment availability to patients. It's a very sophisticated area that you have to know how to navigate. We could navigate through this phase with the guidance of one of our officers and advisors, Tomasz Zastawny, DSc, Ph.D., who specializes in the design and execution of human trials. Investors, however, would just as well see us partner with a major Pharma company to take our therapy through human trials. Even if there was an acquisition that would probably be advantageous for investors. Our fund raise is through the offer to investors of a SAFE (Simple Agreement for Future Equity) with a cap on our company valuation at $10 million. We have a current appraisal from Navigant Consulting that calculates our present value at $126 million. At a $126 million valuation, an investor would realize a 12 times appreciation in his/her investment. I see that happening, and we would welcome it. However, for investors, any future valuation over $10 million results in a successful investment. We have companies watching our progress and have expressed an interest in discussions once we complete testing of the recombinant or completing of animal trials. That's our goal, and I think that's a good goal for the investors as well.

Who is on your team?

My brother, Dr. Joseph Cotropia, M.D., is clearly more knowledgeable in this field than other scientists and biotech researches that we've ever encountered. Dr. Gaurav Chandra and Dr. Seth Sheiner, both M.D.s, are officers and advisors. Our scientific advisory board includes leaders in their field and include: Ellen S. Vitetta, Ph.D - Dr. Vitetta is Professor of Immunology at the University of Texas Southwestern Medical Center and a Distinguished Teaching Professor at the UT Southwestern Academy of Teachers. She is also the Scheryle Simmons Patigian Distinguished Chair in Cancer Immunobiology and Director of the Cancer Immunobiology Center at UT Southwestern Yvonne J. Bryson, M.D.Dr. Bryson has served as a Professor of Pediatrics and Chief, Division of Pediatric Infectious Diseases, David Geffen School of Medicine, Mattel Children's Hospital at UCLA, Marian Davies Children CenterLos Angeles, California Dalila B. Corry, M.D.Dr. Corry has served as Professor of Clinical Medicine, Chief, Division of Nephrology, David Geffen School of Medicine at UCLALos Angeles, California

What is your growth strategy?

Therapeutic antibodies have come of age. They are the fastest growing segment of pharmaceutical industry, rising from $26 Billion in sales in 2007 to $44 Billion in 2015 with the expectation of growing at a 10% rate each year though 2020. We are in the heart of this trend in therapies. We are making great progress through use of specialist laboratories who we have engaged. For example, the light chain and the heavy chain have been sequenced by a specialty lab in Boston, STC Biologics, and is being confirmed by Rapid Novor of Canada. The next phase of testing will be completed with a long-term partner we have at the Univ. of South Florida. Dr. Cao’s lab is imminently qualified to test our antibody using multiple real-world virus specimen. In contrast, in many cases those in the industry are testing their anti-HIV antibodies against what are called "pseudo" viruses. These are laboratory created HIV viruses which are not indicative of the actual virus that people in the world contract. You have to know which lab can do these tests correctly, and Univ. of South Florida is one of them, Boston University is another. Animal trials will be conducted at the MD Anderson Keeling Center in Bastrop, Texas, which is an animal trials facility. They're experts in their field. What qualifies us is the fact that we know who in the field can do the each step correctly. Additionally, we recognized that monoclonal antibodies can be combined to improve results. Our antibody can be combined with others to improve effectiveness. When we visit with other companies, they're not thinking in those terms. The analogy I use is, if you were a firetruck at a huge fire and another firetruck pulled up, would you tell the second truck to go home or would you tell them to join in? You'd tell them to join in, because your pumps might fail, or you might not have the optimum fluids for the type of fire you face. Our monoclonal could be combined with others, and others could be combined with ours if needed. You have to know what you have, how to apply it, and how to achieve effective results in patients. We don't think that another monoclonal would have to be combined to ours, but two fire trucks are better than one. We've seen a lot of sophisticated groups who have said they have the solution but none have demonstrated successful results. The Merck and NIAID failed HIV vaccine in 2007 is a prime example of a failed approach. More, recently, the promising anti-gp120 bNAb 3BNC117, demonstrated successful human CD4 binding site block-age, but ultimately HIV viral escape was observed after single therapy, specifically as gp120bs is conformational and gp120 is hypervariable and mutable.4,5 Another failed clinical study published within the last few months (Bar KJ, et. al., 2016) studied a bNAb VRC01, that similarly interfered with HIV CD4-binding to gp120. The results of this study demonstrated a median time to viral rebound of only 4 weeks.6 Both VRC01 and 3BNC117 were observed to exert pressure on the rebounding virus, resulting in restriction of recrudescent vi-ruses and selection for preexisting and emerging antibody neutralization–resistant virus.6,7 These and other attempts to develop vaccines targeting gp120 have failed, for reasons including insufficiently potent neutralizing antibodies (nAbs) against gp120 along with hypermutability of the virus for that specific glycoprotein. There have been too many misses and not enough well thought through approaches. We believe we have an approach that deserves to be carried forward. HIV is one of those things that everybody knows about. It may have lost some of its headline shine that it used to get in the '80s and '90s, but it's still a pandemic, and perhaps still more of an issue in a lot of the developing countries. One reason why a cure hasn't been successful is that big drug companies would be financially hurt by a cure because HIV is a money maker. Big pharms companies sell $17 billion a year in antiretrovirals, so they don’t have an interest in seeing that disturbed, which a cure would actually do. While our therapy will result in financial reward, more importantly it will save lives and is clearly a feel-good type of investment. That you have the potential to so significantly help people, men, women and children, to live without HIV is a rewarding feeling. Our technology gives an investor the opportunity to disrupt something that's been going on for decades. And significantly, our treatment can be used as a preventative barrier for mother-to-child HIV transmission. One should realize that 400 children die every day from HIV, almost twice the number that die from cancer. We don't see that magnitude in the U.S., but worldwide it is a horrifying statistic, which people just don't focus on.

What do you estimate your treatment will cost?

It has been estimated that treatment could cost as little as $20,000 per patient. Whatever the cost is, it will be far less that the $380,000 which is what patients pay now for a lifetime treatment using antiretroviral drugs. While we don’t know precisely where the price will end up, it’s going to be dramatically less expensive than what patients are paying now.

What's your cash flow?

Cash on hand - $19,700. Our monthly overhead is less than $3,000 per month. We have commitments from our principals for funding as needed for operations. Thus, we have an unlimited runway. We have an SBIR NIH grant application pending in which potential funding (a successful award would be $600,00 over a 2 year period) will be announced later this year.

1	We have created a cell line that produces an anti-HIV antibody called Clone 3.
2	We have demonstrated that Clone 3 neutralizes all clades and groups of HIV isolates.
3	We have identified that Clone 3 targets HIV at an immutable site on the HIV virus.
4	We expect to complete animal trials within 18 to 24 months.
5	We are working with several world-class laboratories who will assist us in conducting the next steps of our plan.
6	1.2 million estimated people die from HIV each year.
7	2 million estimated people are infected with HIV each year.

1	The next 3 steps in our development of our anti-HIV monoclonal antibody (Clone 3) are to (1) create the recombinant of the Clone 3 antibody in a CHO cell line and produce a sufficient quantity of the recombinant for testing, (2) test the recombinant Clone 3 against a full panel of HIV isolates (strains of the virus) and thereafter (3) conduct macaque animal trials to demonstrate the effectiveness of the antibody in an animal study. In these steps, possible difficulties can arise such as: difficult or delay in creating a successful CHO cell line; the created cell line only being transient and not a stable permanent CHO cell line; the cell line secreting non-biologically active recombinant antibody; or the CHO cell line not secreting a sufficient quality or quantity of antibody. Once the recombinant cell line is produced, the resultant antibody may not demonstrate the same effectiveness against HIV isolates tested as has the parent cell line produced monoclonal antibody. In the macaque trials, the results may not be full validation of the neutralizing capability of the Clone 3 antibody previously demonstrated as fully neutralizing in in vitro tests.
2	Though most of the officers are full time, the following officer is part time: Gaurav Chandra, M.D., FAGE, MBA, Vice President of Research and Development.
3	While it is unlikely, patent protection that we expect to secure may be limited or may not prevent another company from circumventing our technology. If this were to occur, then a competitor may produce a similar therapy that prevents the successful adoption and sale of ourmonoclonal antibody. In this event, our profit potential would be adversely effected.
4	Our technology might not be as effective as other monoclonals developed in the future. If this were to occur, then our monoclonal would be competing with more effective therapies and would be less likely to produce revenue.
5	The cost to complete human trials will be large and we will need to partner with pharmaceutical companies to complete such trials. Difficulty could arise in these negotiations. If there were to occur, the pharmaceutical bidders might place a low valuation on our technology on the basis that further human trials and bring-to-market costs are so great.
6	Human trials might not produce the favorable results we expect. If this were to occur, our monoclonal would not likely be accepted in the market place as a viable therapy.
7	Other therapies might compete with our approach and limit the financial return. There might be several alternatives to our therapy and thus this would limit our profit potential or the valuation of our technology. However, a combination of therapies is often used in patient treatment for most all diseases.
8	As a biotech company that relies on specialized outside labs to conduct some phases of our development work, their actions and/or unauthorized use of proprietary technology or patented components might affect the resulting products produced under contract for us. If this were to occur, then our final product may be subject to a claim of rights by other parties with whom we have no direct contact.
9	Our reliance on outside specialized labs also could result in delays in advancement due to problems occurring in these labs over which we have no control. Such situations could delay our development significantly or might prevent successful progress altogether.
10	Because we use multiple specialized outside labs to confirm final efficacy, contradictory results can result, causing delays and uncertainty regarding the optimum final product.
11	Officer Gaurav Chandra is not currently full time with the company. As such, it is likely that the company will not make the same progress as it would if that were not the case.
12	In 2015, Dr. Joseph Cotropia, a director and officer of BioClonetics had hisTexas medical license revoked by the Texas Medical Board. The California Medical Board followed the action of the Texas Medical Board and revoked Dr. Cotropia’s California medical license. In its revocation action, the Texas Medical Board alleged that Dr. Cotropia failed to have written protocols in place for mid-level providers working under him and failed to document his supervision of these providers. All the allegations of wrongdoing made the Texas Medical Board have been and are challenged by Dr. Cotropia. The revocation decision is now on appeal before the Texas 8th Court of Appeals, No. 08-16-00056-CV. Dr. Cotropia expects to prevail in this appeal. However, these facts and appeal are not considered by the Company to have an impact on the Company’s current work and focus on providing a therapy for HIV through the use of the Company’s monoclonal antibodies. Dr. Joseph Cotropia holds a Bachelor of Science degree in Chemistry, a Master of Science degree in Physiological Chemistry and a Doctor of Medicine degree from the University of Texas Southwestern Medical School, Dallas, Texas. From receipt of his Doctor of Medicine degree in 1973, Dr. Cotropia’s focus has been on research in the field of biochemistry and particularly in the field of therapeutic monoclonal antibodies. Dr. Cotropia has also served as a practicing physician.

Director	Occupation	Joined
Joseph P. Cotropia	Researcher @ BioClonetics	2009
Gaurav Chandra	Physician @ GlobeMD	2014
Charles S. Cotropia	Attorney @ BioClonetics	2009

Officer	Title	Joined
Joseph P. Cotropia	Chief Science Officer, Director	2009
Paul D. Fellegy	Secretary, Treasurer, CFO	2009
Gaurav Chandra	COO, Vice President Research and Development	2014
Charles S. Cotropia	CEO, President	2009

$200,000	This level of funding will fund the completion of the production of the recombinant of the Clone 3 antibody for use in in-vitro testing and animal trials.
$400,000	This level of funding will fund the testing of the recombinant antibody against HIV isolates (strains of the virus) leading to animal trials.
$700,000	This level of funding will fund the design and initiation Macaque animal trials to validate the effectiveness of our monoclonal antibody.
$1,000,000	This level of funding will fund the completion of animal trials to validate the effectiveness of our monoclonal antibody in an animal model.

Class of Security	Securities (or Amount) Authorized	Securities (or Amount) Outstanding	Voting Rights
Debt Securities	0	0
Other	0	0
Common Stock	100,000	30,000	Yes

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Current Treatment for HIV is Toxic and Expensive

Antiretroviral chemothereapy (ARV) is currently used to suppress HIV symptoms—but require lifelong treatment and can have major consequences.

On Our Way to a Cure for HIV

We've created an antibody that targets & neutralizes infectious diseases like HIV.

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Clone 3 is what’s known as a monoclonal antibody—a laboratory-made molecule produced by repeated replication of a single parent cell.

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Joseph P. Cotropia applied to Wefunder

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