CEL-SCI ($CVM): The Science Behind Multikine And Why It Is A Dream Platform for Big Pharmas
CEL-SCI ($CVM): The Science Behind Multikine And Why It Is A Dream Platform for Big Pharmas
"Intelligence without ambition is a bird without wings." - Salvador Dalí
Dream Caused by the Flight of a Bee, 1944 - Salvador Dalí
BEFORE STARTING
Some readers have asked me if I’m working for CEL-SCI. No.
Please read the introduction page. I am passionate about investing in general and biotech in particular. As a CEL-SCI shareholder, I have come to define myself as an unabashedly strong believer in Multikine and its positive impact on cancer patients.
The share price and its current fluctuation represent a side show of little interest to me at the moment. If the share price drops, I will happily buy more. What bothers me most are the lies, told by some, which aim to denigrate if not destroy this company in order to fleece those retail investors whose lack of biotech sophistication makes them ill equipped to understand how special is what CEL-SCI has accomplished.
That’s why I write articles to share verifiably good information and analysis. I’m not paid to do so by CEL-SCI nor anyone else.
INTRODUCTION
Grab a cup of coffee. For good measure, maybe two. This article is extensive and chock-full of scientific content. It will explain not only how Multikine activates the immune system to fight cancer but why it is such an extraordinary platform likely to cause any big pharma caring about immunotherapy to salivate and dream of owning.
Multikine is a cocktail of 14 different Cytokines. Cytokines are chemicals generated by cells which act as messages sent between the cells of the immune system to coordinate actions to fight disease.
To understand why Multikine is such a brilliant idea, one will need at least some basic understanding of how the immune system works, a major topic in and of itself. But let’s dive in this big lake of human knowledge.
IMMUNE SYSTEM 101
Our immune systems work together like a football team to defend ourselves against invaders. There are three main systems:
The Complement System which has existed in the living body for hundreds of millions of years.
The Innate Immune System, which exists in most animals, is a “hard-wired” system that helps defend quickly and effectively against common attacks.
The Adaptive Immune System, which exists in vertebrates such as ourselves, is a “software-based” system that adapts itself to defense “on-demand” against more rare attacks.
The stage is set with many players with different roles and complex interactions. So let’s dig further.
THE TEAM AND THE PRINCIPAL PLAYERS
THE COMPLEMENT SYSTEM
The complement system is composed of around 20 different proteins that work to destroy invaders and signal to alert other immune system players that the attack is going on. This system is very old, having existed even in sea urchins about 700 million years ago.
THE INNATE IMMUNE SYSTEM
The main players of the Innate Immune System are killer cells called Phagocytes and Natural Killer (NK) Cells.
Phagocytes. As many medical terms, this word derives from Greek. “Phago-” means “eating”, “-cyte” means “cell”. So Phagocytes basically means “eater cells”. There are 2 of them: Macrophages and Neutrophils.
Macrophages (big eaters) are sentinel cells which live and work just below the surface in all areas of our body exposed to the outside world which are prime targets for microbial infection. Macrophages exist in three stages of readiness:
Resting. In this stage, Macrophages work as garbage collectors, exploring for and cleaning up dead cells.
Activated when Macrophages receive signals that there are intruders in the area. They search for, find and eat the invaders, and subsequently display fragments of invaders' proteins on their surface for other cells to see. A number of signals can activate a resting Macrophage and the most well-known is a Cytokine called Interferon Gamma (IFN-γ). IFN-γ is a very important Cytokine. In addition to activating Macrophages, it also stimulates other killers including Neutrophils and Natural Killer (NK) Cells. Guess what? IFN-γ is part of our Multikine cocktail.
Hyperactivated states occur when Macrophages receive a direct signal from an invader. In this stage, the eating machines function at full power. They also produce and secrete other Cytokines such as Interleukin-1 (IL-1) and Tumor Necrosis Factor (TNF). IL-1 and TNF can help activate other immune system warriors. In addition, TNF can kill tumor cells and virus-infected cells. IL-1 and TNF are both parts of Multikine.
Activation is a very important notion. In general, cells need to be activated to function in an attack. Otherwise, they will simply perform their boring chores or aimlessly dogpaddle through the bloodstream without doing anything of significance.
Macrophages are usually able to deal with small attacks. However, when invaders are numerous, they call for backup. Most common reinforcement is from “on-call” professional killers known as Neutrophils. There are about 20 billion of them in our blood stream, representing about 70% of circulating white blood cells. While rolling through our blood, they sniff for battle signals and when they receive one, they exit the bloodstream, enter into tissue and begin to attack and kill. They are extremely voracious. Their chemicals are so strong that they can cause damage to normal tissues. That’s why Neutrophils are programmed to short-live for about 5 days. Like Macrophages, Neutrophils can also produce battle-ready Cytokines such as Tumor Necrosis Factor (TNF). As you will discover later, Neutrophils play a key role in Multikine’s mechanism of action.
Natural Killer (NK) Cells fall within the final category of killers of the Innate Immune System. Like Neutrophils, NK Cells mainly reside in the bloodstream but enter tissues when there is a battle in progress. NK Cells can destroy some tumor cells, virus-infected cells, bacteria, parasites and fungi.
They destroy these enemies by forcing them to commit suicide. There are several ways to do that. For instance, NK Cells can inject "suicide" enzymes (e.g. granzyme B) into the target. In other situations, a protein called Fas ligand on the NK Cells surface interacts with a protein called Fas on the surface of its target, signaling the target cell to self-destruct.
Natural Killer (NK) Cells identify the target to kill by measuring the relative strength of the Kill / Don’t Kill signals that they receive. The Kill signal is based on interaction between the receptors (a sensor, or antenna) on the surface of NK Cells and the unusual carbohydrates or proteins on the surface of a target cell. The Don’t Kill signal is based on inhibitory receptors that recognize Class I Major Histocompatibility Complex (“Class I MHC”) molecules that are found on most of the healthy cells of the body. This is a very smart way to decide which target to kill, because it helps avoid killing healthy cells which express Class I MHC.
Interestingly, tumor cells always lack or only express low levels of Class I MHC, making NK Cells a perfect killer of cancer tumor cells. As we will see later on, NK Cells play a key role in the mechanism of action of Multikine.
Like Macrophages, NK Cells exist in several states of readiness. When activated, they can produce larger quantities of Cytokines and kill more efficiently. Natural Killer (NK) Cells can be activated by Interferon Alpha (IFN-α) or Interferon Beta (IFN-β), both are mostly produced by a type of white blood cell called Plasmacytoid Dendritic Cell (pDC).
THE ADAPTIVE IMMUNE SYSTEM
If the Innate Immune System protects us against common invaders, the Adaptive Immune System can adapt to defend against specific invaders. This system is based on 2 main types of blood cells: B Cells and T Cells. They are assisted by the messenger Dendritic Cells which create a bridge between the Innate and Adaptive Immune Systems.
B Cells are blood cells that mature in Bone Marrow (that’s where the B comes from) into Plasma B Cells which are factories of Antibodies.
Antibodies are Y-shaped proteins which allow cells to better recognize and attack invaders. They have two parts, the “hands” and the “tail”. The “hands” portion is variable and binds to a specific antigen expressed on the surface of a specific invader. The “tail” portion is fixed and can bind to our killer cells such as Macrophages. So Antibodies do not kill, they simply provide the bridge between the killer and the victim.
Antibodies are powerful tools but don’t work in certain situations, such as when a virus enters a cell. There is no way for Antibodies to enter a cell and bind to a virus. In such situations, T Cells come into play.
T Cells are produced in the Bone Marrow but mature in the Thymus (thus the “T” derivation). T Cells mostly circulate in the bloodstream and only approach tissues when they are called upon to attack.
There are three types of T Cells: (1) Killer T Cells can kill targeted cells by making contact with the infected cells and triggering a suicide, similar to NK Cells; (2) Helper T Cells are factories of Cytokines which help coordinate the battle; and (3) Regulatory T Cells which keep the immune system from overreacting.
On their surface, T Cells have antibody-like molecules called T Cell Receptors (TCRs) that can recognize Antigens. However, T Cells can only recognize an Antigen if it is "properly presented" by another cell. But how is an antigen presented to T Cells? That’s the role of the Major Histocompatibility Complex (“MHC”). There are 2 classes of MHC molecules: Class I MHC and Class II MHC.
Class I MHC is found on the surface of most cells in the body. It acts like a “screen” showing Killer T Cells what’s going on inside these cells. For instance, if a cell is infected by a virus, fragments of the viral proteins are loaded onto Class I MHC molecules and transported to the surface of the cell.
Class II MHC molecules also function as a “screen” but are for Helper T Cells. Only certain cells, such as Macrophages or Dendritic Cells, can make Class II MHC. They are called Antigen Presenting Cells (“APC”).
T Cells mostly circulate around the blood stream and they are activated when an antigen is presented to them. So if the invasion starts in the tissues, how do T Cells, which circulate in the blood, know that something is amiss within the tissues?
That’s when one of the most important players of the immune system comes into play: the Dendritic Cells.
Dendritic Cells don’t kill but act as messengers. When a battle is undertaken in the tissues, Dendritic Cells are activated by battle signals such as Cytokines or chemicals given off by dying cells. Typically, they remain on the battlefield for about six hours to collect samples of battle antigens. Then, Dendritic Cells travel to the nearest lymph node, where they meet with T Cells and activate them with the antigens collected (the lymph node is akin to the meeting place where the Adaptive Immune System is activated). When Killer T Cells are activated, they start proliferating and approaching the battlefield in the tissues in order to kill off the invaders. When Helper T Cells are activated, they begin producing Cytokines to activate other warriors of the immune systems, and also the B Cells which will produce antibodies.
It is clear that the weapons of the immune system are very powerful. For that reason, it must be restrained to avoid the negative repercussions of becoming overly-exuberant. There are 2 mechanisms worth mentioning here:
A type of T Cell called Inducible Regulatory T Cell (iTreg) produces Cytokines such as IL-10 or TGF-β that help restrain the system. IL-10 makes it more difficult for Antigen Presenting Cells to be activated while TGF-β reduces the proliferation rate of T cells and makes Killer T Cells less cruel.
A molecule called Programmed Death 1 (PD-1) helps deactivate Killer T Cells. After activation, the expression of PD-1 increases. The ligand for PD-1 called PD-L1 appears on inflamed tissues. They bind to PD-1 and make Killer T Cells function less well.
Killer T Cells are very hotly researched killers of cancer cells. Multi-billion dollar drugs such as Keytruda or Opdivo are based on the inhibitor of PD-1 of Killer T Cells, making them kill for a longer time. Chimeric Antigen Receptor (CAR) T-Cell Therapy is also an extremely hot topic. Interestingly, CEL-SCI made the choice to virtually ignore Killer T Cells in Multikine’s mechanism of action, relying more on Innate Immune System killers such as Neutrophils and NK Cells. As will become apparent this turns out to be a prescient choice when it comes to cancer treatment. To understand this better, let’s begin by examining how cancer works.
WHY IS IT SO HARD TO CURE CANCER?
WHAT IS CANCER?
In his Pulitzer-winning book “The Emperor of All Maladies: A Biography of Cancer”, Siddhartha Mukherjee provides the following definition of cancer:
Cancer, we now know, is a disease caused by the uncontrolled growth of a single cell. This growth is unleashed by mutations—changes in DNA that specifically affect genes that incite unlimited cell growth. In a normal cell, powerful genetic circuits regulate cell division and cell death. In a cancer cell, these circuits have been broken, unleashing a cell that cannot stop growing.
So in a nutshell, cancer is a disease resulting from broken control systems. There are 2 types of them:
Proliferation systems which promote cell growth; and
Safeguard systems which protect against abnormal cell growth.
Under normal circumstances, proliferation is necessary for human life. For instance, the cells in your heart proliferate until your heart attains the proper size, then they stop proliferating. On the contrary, your skin cells must proliferate almost continuously to replace cells on the surface which are eroded by wear and tear. The control system insures that the proliferation occurs in proper proportions, right place and right time.
However, this growth-promoting system occasionally malfunctions, allowing a cell to grow abnormally. This malfunction is usually caused by mutations that affect the genes that incite unlimited cell growth, and the mutations happen a lot. On average, a cell in your body suffers about 25,000 mutational events every day.
To protect against malfunctions of the growth-promoting systems, your body is equipped with two general types of safeguard systems:
Repair system that helps prevent mutations; and
Guard systems that deal with mutations once they occur.
The repair system works non-stop to repair DNA damage in order to prevent mutations and it usually works well. However, when there are too many mutational events, the repair system may miss one mutation, that is when the guard system is activated. If the mutations are not extensive, the guard system stops the cell from proliferating to provide the repair system more time to work. However, if the genetic damage is too severe, then the guard system will trigger the cell to commit suicide.
When both growth-promoting and safeguard systems are corrupted within a cell, nothing can stop the cell from proliferating and cancer occurs.
TYPES OF CANCER CELLS
Cancer cells can be classified into two general groups:
Blood cell cancers; and
Non-blood cell cancers, also called solid-tumor cancers.
All blood cells are born from blood stem cells in the Bone Marrow. They grow through various stages, before maturing into fully-functioning blood cells such as red blood cells or white blood cells (e.g. Neutrophils, NK Cells, B or T Cells). Blood cell cancer arises when blood cells stop maturing at an intermediary stage and start proliferating. These immature cells then fill up the bone marrow, preventing it from producing cell bloods or other cell bloods from maturing. A blood cancer patient then usually dies arising from the lack of red blood cells, or because of infection due to the lack of white blood cells.
Solid tumor cancers can have two sub-types: carcinomas and sarcomas. Carcinomas are cancers of epithelial cells which line the outer surfaces of organs and blood vessels throughout the body, as well as the inner surfaces of cavities in many internal organs. These cancers generally kill by metastasizing to a vital organ, where they grow and crowd the organ until it can no longer properly function. Sarcomas are cancers of the connective and structural tissues. They are relatively rare compared to carcinomas. For instance, 90% of the head and neck cancers are squamous carcinomas of the head and neck, the target indication of Multikine. And squamous cells are just a subset of epithelial cells.
As target indications of Multikine are solid tumor cancers, our focus turns only to these cancers in the next section.
WHY IS IT SO HARD TO KILL SOLID TUMOR CANCER CELLS?
As explained in the previous section, our body has a powerful immune system with an army of messengers, eaters, fighters, and killers. So why does it allow cancer cells to grow? Let’s explore the problems presented here:
PROBLEM #1: ACTIVATION
When cancer arises, our first line of defense is the innate immune system with our big eater friends, Macrophages. The problem is: without being activated, those Macrophages just remain in their resting stage and circulate collecting garbage. They may pass by cancer cells without recognizing them. Macrophages need to be activated before they can kill cancer cells. For instance, to treat bladder cancer, patients receive injections of bacille Calmette-Guérin (BCG), a cousin of the bacterium that causes tuberculosis. BCG hyperactivates macrophages, allowing them to kill the cancer cells.
What about other killers and Killer T Cells, NK Cells or Neutrophils? The problem is even worse. Those killers are mostly circulating in the blood and rarely go to tissues where the tumor is located unless they are activated through the reception of a clear signal that a battle is on-going.
PROBLEM #2: MUTATION
A possible scenario in which Killer T Cells can be activated would be when the primary tumor metastases to a lymph node where a Killer T Cell is residing. But a new issue arises. Cancer cells mutate like crazy and some of these mutations may escape recognition by an activated Killer T Cell. For instance, tumor cells have been known to mutate so that they stop producing the particular Class I MHC molecules that Killer T Cells require to recognize them. So even when Killer T Cells are activated, it is possible that they do not see cancer cells since the “screen” on the surface of cancer cells has been removed via mutations.
PROBLEM #3: CANCER CELLS FIGHT BACK
It is not for nothing that cancer is called the emperor of all maladies. Cancer cells are extremely intelligent and find many ways to fight the immune system back.
For instance, many cancers “hack” the tolerance mechanism of activated T Cells. As seen in the previous section, activated T Cells have many inhibitory receptors PD-1 which are generally responsible for preventing the immune system from attacking the body's own tissues. Normally, the PD-1 receptor on activated T Cells binds to ligands PD-L1 or PD-L2 on other cells, deactivating a potential T-cell-mediated immune response against normal cells in the body. Many cancer cells make proteins such as PD-L1 that bind to PD-1, thus shutting down the ability of Killer T Cells to attack the cancer cells.
Keytruda and Opdivo, two of the best sellers in oncology are based on this phenomenon. They work by inhibiting PD-1 on the lymphocytes, preventing it from binding to ligands that deactivate an immune response, allowing the immune system to target and destroy cancer cells. However, this mechanism has a huge downside as it breaks the self-tolerance mechanism and allows the immune system to attack the body itself!
Tumors also modify their surrounding environment to make it more difficult for Killer T Cells to operate. For example, many tumors express high levels of indoleamine 2,3-dioxygenase. This enzyme results in a rapid consumption of tryptophan from the tumor environment. This makes Killer T cells starve from tryptophan and stop proliferating.
So, bottom line, it’s very hard to fight cancer. Killer T Cells, the “hyped” Killers, are actually not very well-positioned to fight solid tumor cancer. They are not near the cancer cells in the tissues; cancer cells mutate to escape from them; cancer cells create a surrounding environment which does not welcome Killer T Cells and cancer cells can shut them down through the PD-1 / PD-L1 pathway.
CEL-SCI has chosen a different path: to not rely on Killer T Cells. Let’s examine its approach and how it works:
MULTIKINE, BIG PHARMAS’ DREAM PLATFORM
HOW DOES MULTIKINE WORK?
In late stage solid tumor cancer, there is typically a primary tumor as well as micro-metastases around the tumor and the lymph node. Micro-metastases are thought to be the main cause of cancer recurrence.
Multikine is injected around the tumor (not in the tumor) and in regional lymph nodes. Its objective is to clear the local and regional tumor metastases and provide a clean tumor margin to improve the surgeons’ abilities to easily remove all of the tumor.
Multikine is mainly composed of 14 different Cytokines shown in the table below:
To simplify, those Cytokines can be classified into 3 families:
Cytokines such as TNF-α and IFN-y which can directly kill cancer cells.
Lympho-proliferative Cytokines such as IL-1, and IL-2 which promote growth of white blood cells; and
Chemotactic cytokines such as IL-6, IL-8 and MIP-1α which stimulate recruitment of cells to specific locations.
Multikine activates the immune system to kill cancer cells in four main steps:
Tumor-killing Cytokines directly attack the tumor cells, causing them to release tumor antigens.
The Dendritic Cells collect tumor antigens, transport them to near-by lymph nodes, and present them to T Cells. Combined with Multikine’s white blood cell growth-promoting cytokines, this induces replication of tumor-specific T-cells to target cancer in the lymph nodes and prepare them for recruitment to the tumor site.
Then, Multikine’s chemotactic factors recruit anti-tumor specific Helper T Cells from the local lymph nodes. As seen before, the tumor appears to be able to shut down Killer T Cells in its neighborhood but this does not seem to be the case for Helper T-Cells. The tumor-infiltrating Helper T Cells generate a local anti-tumor response. Helper T Cells notably help activate NK Cells which are well positioned to kill tumors as tumor cells always lack or only express low levels of Class I MHC (reminder from previous section: NK cells can kill cells with low levels of Class I MHC expression).
Lastly, when the battle is going on, Neutrophils circulating in the blood can detect the fight signal and join. Other Cytokines in Multikine, or those secreted on‐site in the tumor microenvironment by the tumor‐infiltrating lymphocytes, induce local fibrosis.
Multikine has been brilliantly designed to overcome the three problems posed by cancers:
The Activation Problem: By having a first crude attack using tumor-killing cytokines, Multikine forces cancer cells to release antigens. These antigens are like the “keys” collected by Dendritic Cells to activate the immune system, starting with T Cells in the lymph nodes. A very smart tactic!
The Mutation Problem: As previously discussed, cancer cells keep mutating to hide from Killer T Cells by removing expression of Class I MHC molecules. Multikine does not rely on Killer T Cells but on Neutrophils, and NK Cells which can efficiently kill targets which lack Class I MHC molecules. Clever choice!
Cancer Cells Fight Back: As explained in the previous section, the cancer tumor creates an environment which shuts down Killer T Cells, but this does not seem to work on Helper T Cells. Multikine leverages Helper T Cells to infiltrate the tumor environment in order to trigger a local tumor response (e.g. calling on NK Cells and Neutrophils). By doing this, Multikine also mitigates the conflict between self-defense and self-tolerance of Killer T Cells, encountered by checkpoint inhibitor drugs such as Keytruda or Opdivo. That differentiates Multikine as “safe” compared other competitor drugs which too often induce cells counterproductively to attack the patient’s own body. Brilliant idea!
Interesting? Multikine mostly ignores Killer T Cells only uses the Helper T Cells from the Adaptive Immune System to coordinate the battle but the main killers of cancer cells are actually NK Cells and Neutrophils, all from the Innate Immune System. This turns out to be a brilliant strategy to get around the 3 problems posed by cancer and make Multikine both effective and safe.
WHY IS MULTIKINE A DREAM PLATFORM FOR BIG PHARMAS?
Given your current understanding of how Multikine works, there should be no surprise as to why it is such a dream platform:
#1: SAFETY FIRST
During its Phase 2 and Phase 3 trials, there were no safety issues found with Multikine. This is totally understandable since Multikine is formulated as a mixture of cytokines which exist naturally in our body and a reasonable dose of those cytokines has been shown to cause 0 safety issues.
This is a big advantage compared to existing immunotherapies such as checkpoint inhibitors like Keytruda or Opdivo. As noted above, once the PD-1 checkpoints are inhibited, the self-tolerance mechanism is broken and Killer T Cells can attack the patient’s own body, injuriously killing normal cells!
#2: FIRST LINE TREATMENT
As an immune system booster, Multikine works best when the immune system is still intact and healthy, i.e., before other treatments. This is very significant since, by definition, a first line treatment addresses a larger population than any second, third or fourth line treatments.
Merck and BMY would dream to have Keytruda and Opdivo as first-line treatments but it is next to impossible for their drugs to be employed in such a fashion. Why? Because both Keytruda and Opdivo allow the immune system to attack the body. Imagine infusing those drugs into a healthy immune system! Therefore, the only credible way for these two Pharmas to possess a powerful and safe first-line cancer treatment would be to buy Multikine or its company, CEL-SCI.
#3: ONE PLATFORM, FULL PIPELINE
Although Multikine addresses head and neck cancer as its initial target for tactical reasons (severe unmet medical need), there is nothing in Multikine’s treatment which is specific to head and neck cancer. The same mechanism of action to boost the immune system can be administered to other solid tumor cancers such as melanoma, cervical dysplasia/neoplasia, as well as breast, skin, bladder, and prostate cancers. Those are huge markets. For instance, according to Globocan, there are more than two millions new cases of breast cancer per year, 1.4 million for prostate cancer. In addition, given its excellent safety profile, Multikine can proceed straight to Phase 2 / 2b for other indications in the future.
#4: EXTREME FLEXIBILITY
In its Phase 3 trial, Multikine was administered over a three week period before surgery to head and neck cancer patients, in order to respect the standard of care (SOC) guideline. This is actually an extremely constraining method of administration but CEL-SCI had no choice. They needed a standardized treatment for the trial which would neither delay nor disrespect the SOC.
Once Multikine is approved by the FDA, there will be numerous ways to test Multikine in order to determine its true power:
What if Multikine were administered not only during 3 weeks but 4, 5 or even 6 weeks before surgery?
What if Multikine were also to be administered after surgery / or surgery and radiation? Since Multikine is a “safe immune booster,” why not use it anytime we need to boost the immune system?
In addition, for future indications, the Multikine’s mixture could be modified to reflect researchers’ best knowledge about cytokine’s benefits. Overall, Multikine offers a very flexible platform with which doctors and researchers will like to play.
#5: SCALABILITY
Multikine is an off-the-shelf product. The choice of mixing cytokines is brilliant. Cytokines are messages used to direct the immune system and cytokines do not differ from one patient to another.
Therefore, compared to other autologous therapies (e.g CAR-T), the treatment journey of Mulikine is much simpler, and the production of Multikine can offer a significant cost advantage to its owner.
CONCLUSION
Product, product, product. Medicine, medicine, medicine. Drug, drug, drug.
The most important element of any investment thesis should be the company’s “product,” in this case CEL-SCI’s drug: Multikine. Through thorough examination of it in this article, we have come to the conclusion that CEL-SCI has developed a superb and unique strategy to attack cancer by focusing on Cytokines.
Those molecules direct the immune system, are naturally produced by the body and do not require any personalization. The mechanism of action of Multikine demonstrates that the immune system can circumvent the defense mechanisms of the cancer tumor which generally focus on shutting down Killer T Cells. CEL-SCI made a different choice compared to other mainstream immunotherapies which put Killer T Cell at the heart of their treatment thesis, and we believe CEL-SCI’s choice, however long it has taken, will be proven not only to have been smart but also to surpass the competition and become the gold standard of currently available immunotherapies.
Now CEL-SCI seems to have borne fruit with its momentous Phase 3 results on a significant part of the Head & Neck cancer population. And, we believe this to be just scratching the surface of greater success to come. Its excellent safety profile, aggressive approach to cure many types of cancer as a first line treatment, extreme flexibility and scalability makes Multikine a dream platform for Big Pharmas which are interested in the cancer treatment market.
Anyone hear that knock on the door?
I am curious who the author was of the 21 page article and his/her credentials. Was the article Peer Reviewed or just one person's gathering and summarizing of information from various sources?
Thank you.
The possibilities are unlimited, i have no doubt that it works against lots of cancer types..