Cellceutix Provides Insights to Its Four Clinical Trials

BEVERLY, MA--(Marketwired - August 07, 2015) - Cellceutix Corporation (OTC: CTIX) (the "Company"), a clinical stage biopharmaceutical company developing innovative therapies with oncology, dermatology, anti-inflammatory and antibiotic applications, would like to address shareholders with recent events concerning Cellceutix.

This week we updated shareholders on our clinical programs for the treatment of Prurisol for psoriasis and Brilacidin for the prevention of oral mucositis in patients undergoing chemoradiation in the treatment of head and neck cancer, exciting drugs for areas of great unmet medical need. Regarding the Kevetrin cancer trial, it is an important trial with one patient now entering the eleventh month of therapy. We are planning to finish this study and issue an update as soon as possible. The recent grant of an Orphan Drug status for treatment of ovarian carcinoma gives me the opportunity and pleasure to address shareholders as to why the FDA granting an Orphan Drug designation for Kevetrin may have been a relatively easy decision.

Cellceutix applied for Orphan Drug status for Kevetrin for treatment of ovarian carcinoma in June 2015 and approval was granted in July 2015. Cellceutix' application included nonclinical data on effects of Kevetrin in in vitro evaluations in tumor cells. However, the application also included information for nine patients with metastatic ovarian carcinoma who were among the 40 patients enrolled in the ongoing Phase 1 study of Kevetrin for solid tumors at Dana Farber Cancer Institute and Beth Israel Deaconess Medical Center.

These nine patients (mean age 64 years) were diagnosed with ovarian cancer an average of 6.7 years before beginning Kevetrin therapy at doses up to and including 450 mg/m2 per week. At enrollment, these patients had radiological evidence of spread of their cancer to vital organs -- including liver, kidney, lung, spleen, lymph nodes, as well as peritoneum. All patients had previously received chemotherapy that was not curative and/or did not induce remission.

Patients with ovarian cancer generally have tumors that contain mutated or inactive p53 -- a tumor suppressor gene. Kevetrin has been shown, in vitro, to activate wild-type and degrade oncogenic mutant p53. Expression of p21 is recognized as a marker of p53 activation. Among these nine patients with ovarian carcinoma enrolled in the Cellceutix Phase 1 study, the median change in p21 expression in peripheral blood lymphocytes was an increase of 22% after the first dose of Kevetrin.

During Kevetrin treatment, four of the nine patients with advanced ovarian carcinoma were documented to have stable disease (by radiographic examinations) for 3 to 6 months while receiving Kevetrin.

These preliminary results have spurred Cellceutix to begin planning for a Phase 2 study in patients with ovarian carcinoma that will evaluate different dosing strategies for Kevetrin in the ovarian cancer population.

I have received many emails and questions in response to a ludicrous, rambling and totally inaccurate article about the Company written by people who describe their interest in Cellceutix as "I am/we are short CTIX" (the "Shorter"). As will be shown shortly, the Shorter has no idea what trials Cellceutix is engaged in. It is disheartening to me that some shareholders may have sold their shares based on this article.

The Shorter claims: "Additionally, after hiring an independent scientist with a Doctorate in Biochemistry to review Cellceutix's 'science,' I have concluded that the company's drug pipeline is without merit and is likely entirely without value, as detailed below."

Many companies, including Cellceutix, have been the topic of a bash piece and our typical policy is to ignore it as our science speaks for itself. However, in this case, the egregious article is so fraught with inaccuracies about our drug candidates and biotechnology in general veiled under the pretense that some anonymous so-called expert consulted in review, that it is our responsibility to respond at length to the publisher seeking to have the defamatory article removed.

After reading the following responses by Cellceutix, I believe you'll agree the Shorter certainly did not hire a scientist with a Doctorate in Biochemistry.

Shorter: Cellceutix is run out of what appears to be an empty office building
CTIX claims to operate out of the following address:
100 Cummings Ctr Ste 151b
BEVERLY, MA 01915-6117
This is the company's official address listed in SEC filings.

Cellceutix: Cellceutix Corporation signed a lease extension agreement with Cummings Properties, which began on October 1, 2013. The lease is for a term of five years ending on September 30, 2018, and requires monthly payments of $17,000. (http://www.sec.gov/Archives/edgar/data/1355250/000147793214002418/ctix_ex1039.htm )

Shorter: I obtained photos from this office in early August 2015 during business hours, and it appears empty to me.

Cellceutix: Our offices and research laboratory are part of a two-million-square-foot office complex at Cummings Center in Beverly, MA; this is hardly an empty building. Cellceutix employees are mostly research and clinical personnel that typically are working in the labs behind the offices.

Shorter: Brilacidin is an ineffective antibiotic candidate that causes material side effects in patients.

Cellceutix: The hyper-linked table provided by the shorter is misleading and irrelevant as it focuses exclusively on key Gram-negative bacteria. Brilacidin is for treating gram positive infections such as acute bacterial skin and skin structure infections (ABSSSI) caused by Staphylococcus aureus, including methicillin-resistant strains (MRSA), and was not developed for the treatment of Gram-negative infections.

Shorter: The implications are large and clear -- the biotech community looked at Polymedix's assets and deemed them without value. This is particularly notable in light of the fact that company management owned nearly 15% of the equity, and had every incentive in the world to get a deal done and/or maximize the value of the pipeline.

Cellceutix: Need I remind the shorter of the recent events regarding Pharmacyclics buyout for $21 billion.
http://www.forbes.com/sites/antoinegara/2015/03/05/pharmacyclics-billionaire-top-trade-robert-duggan-abbvie/

It should be added that PolyMedix received over 20 million dollars in competitive grant and contract funding from the NIH, NSF and armed forces to conduct research on brilacidin and other mimics. This served to us as important validation from the scientific community on their approach and progress.

Shorter: The former CEO of Polymedix, who was intimately familiar with these assets, immediately sold all of his CTIX stock (1.4 million shares) acquired in the deal at the earliest possible opportunity.

Cellceutix: A lie and a link meant to mislead investors. No shares were issued to the former CEO of Polymedix. The link is for the issuance of shares to the US Bankruptcy Court for the purchase of Polymedix assets.

http://www.sec.gov/Archives/edgar/data/1355250/000135525013000032/reportpoly_8k.htm

Shorter: Commercial development of antimicrobial peptides (AMP) is really an uphill battle due to high production costs, high susceptibility to intestinal chemicals-induced degradation, and limited treatment effects in recommended dosage that leads to risk of drug overdosage. There are also a host of related side effects, including risk of allergic events, relatively short-duration activity, limited binding with target molecule(s) and a higher rate of elimination from the body.

When we look into the past, Brilacidin was originally developed by Polymedix (PMX-30063) and later acquired by Cellceutix. According to Cellceutix, this drug is a cationic antimicrobial peptide that is similar to naturally-occurring immune system protein that fights bacterial infection (Human defensin peptidomimetic, or HDP).

Cellceutix: The shorter describes many limitations associated with peptides for commercial development as therapeutic agents. However, the shorter is misleading as Cellceutix is not developing peptides as antimicrobial agent,s nor is brilacidin a peptide. Rather, the core of Cellceutix's antimicrobial technology, which originated at PolyMedix, is the development of small nonpeptidic mimics of antimicrobial peptides. The goal is to recapitulate the biological and structural properties of antimicrobial peptides on small chemical backbones without trying to duplicate the peptide structure. If one examines the structure of brilacidin it is clear that it is not a peptide but rather a small amphiphilic compound. This approach was taken to address the very issues the shorter describes for therapeutic development of peptides. These chemical mimics would be expected to have better pharmaceutical properties than peptides due to their small size and improved stability and should be less expensive to produce with selection of appropriate building blocks. Furthermore, synthetic chemistry approaches can be utilized to fine-tune their structures, to a much greater extent than possible by peptide chemistry, to enhance antimicrobial activities and minimize toxicities.

Shorter: When we look into the past, Brilacidin was originally developed by Polymedix (PMX-30063) and later acquired by Cellceutix. According to Cellceutix, this drug is a cationic antimicrobial peptide that is similar to naturally-occurring immune system protein that fights bacterial infection (Human defensin peptidomimetic, or HDP).

Cellceutix: NOT TRUE. Brilacidin is a fully synthetic mimic of "defensing", a type of antimicrobial peptide (AMP), from a class of proteins known as host defense proteins (HDPs). These HDPs are part of the innate immune system. Thus, brilacidin is referred to as a "defensin-mimetic". It can also be called an "HDP-mimic".
http://cellceutix.com/brilacidin/#sthash.BbeXSOq4.dpbs

Note that brilacidin is a synthetic molecule, known in the pharmaceutical industry as a "small molecule". This is in contrast to a much larger "biologic" or protein or peptide, known in the pharmaceutical industry as a "large molecule". This is an important distinction, because there are many technical and functional problems inherent in the creation, manufacturing, and development of large molecules that do not exist for small molecules. Thus, using a small molecule "mimic" of a protein or peptide, rather than the corresponding protein or peptide itself, has some advantages.

In short, brilacidin is not a protein, peptide, biologic or large molecule. This is an important distinction.

Shorter: In recent years, antimicrobial peptide resistance has been emerging as a global public health problem, and remains a serious threat.

Cellceutix: NOT TRUE. "Antimicrobial peptide resistance" (to native AMPs, such as defensin) is a theoretical problem. It is different from "antibiotic resistance", which is a growing public health concern.

Brilacidin, a small molecule, can theoretically remain functional in the face of "AMP resistance", as it is similar, but not identical to, its large molecule counterpart (native AMP). More importantly, it can remain functional in the face of existing "antibiotic resistance". This is because it is from a brand new class of antibiotics to which resistance has not yet occurred. Therefore, it can be used to treat bacteria that are currently resistant to other antibiotics. In addition, given brilacidin's mechanism of action, among other properties, the development of specific brilacidin resistance is very unlikely.

Shorter: Cellceutix has attempted to exploit this problem and reap the benefits. Brilacidin is being hyped as a miracle drug that can overcome antimicrobial peptide resistance, and is reported to be effective against S. aureus and other gram-negative bacteria, including Escherichia coli. In reality, these claims are spurious.

Cellceutix. NOT TRUE. Staphylococcus aureus is Gram-positive -- not Gram-negative. This is an important distinction, as you will see below.

Shorter: As stated by the company, disruption of the bacterial cell membrane (outer wall) is the prime mechanism of action of Brilacidin to kill harmful bacteria, including gram-negative bacteria (more on why this is wrong below). In the Phase II study conducted by Polymedix, the antimicrobial efficacy of Brilacidin (PMX-30063) was compared with daptomycin for treatment of ABSSSI (acute bacterial skin and skin structure infection) due to methicillin-susceptible S. aureus.

When we look into the ABSSSI trial results, out of eight bacterial variants/strains, Brilacidin has no activity against seven strains, including Pseudomonas aeruginosa, certain species of Enterobacteriaceae, Acinetobacter species, including Acinetobacter baumannii -- which are the common infectious organisms that cause serious and life-threatening ABSSSI infections. The results clearly showed Brilacidin's inefficacy against several bacterial strains except for one -- EBSL Enterobacteriaceae.

Cellceutix: NOT TRUE. Again, the hyper-linked table provided by the shorter is misleading and irrelevant as it focuses exclusively on key Gram-negative bacteria. Brilacidin is for treating gram positive infections such as acute bacterial skin and skin structure infections (ABSSSI) caused by Staphylococcus aureus, including methicillin-resistant strains (MRSA), and was not developed for the treatment of Gram-negative infections.

More importantly, in two phase 2 trials, brilacidin was effective in the treatment of ABSSSI caused by the two most important ABSSSI-causing organisms: Staphylococcus aureus (including MRSA) and Streptococcus pyogenes. These data were presented at two global infectious disease meetings (ICAAC 2012, ECCMID 2015), reviewed by numerous infectious disease experts, and served as the basis for FDA allowing Cellceutix to complete phase 2 and begin preparations for Phase 3. http://cellceutix.com/wp-content/uploads/2014/06/A-Randomized-Double-Blind-Study-Comparing-Single-Dose-and-Short-Course-Brilacidin-to-Daptomycin-in-the-Treatment-of-Acute-Bacterial-Skin-Skin-Structure-Infections-ABSSSI1.pdf

Shorter: Inefficacy is not the only problem of Brilacidin. Incidence of sensory nerve symptoms, such as numbness and tingling of the extremities and elevated blood pressure due to unknown problems were reported as serious adverse events in 65-87% of Brilacidin-treated patients. This alone means that the drug is unlikely to get approved, in my view.

Cellceutix: 1) See above comments and link to presentation on Phase 2 data. 2) This is false. These were not reported as "serious adverse events in 65%-87%". In the recent phase 2b study, there were no "serious adverse events" (SAEs) related to either numbness/tingling or blood pressure.

While numbness/tingling were reported, it is not a safety concern. These cases were mild and transient, and the events fully resolved without any intervention -- similar to a Novocain injection by the dentist

Shorter: Our scientific review has shown that Brilacidin is not effective even against EBSL Enterobacteriaceae, unlike what Cellceutix claims. This means that Brilacidin is not effective against any of the eight bacteria strains targeted in the Phase II clinical trial, will almost certainly not be approved, and is essentially without value. In my view, this is why CTIX was able to acquire the failed Polymedix assets at a low price -- because real biotechnology companies knew this drug was likely without value. This is how the drug ended up in an OTC shell run by stock promoters.

Cellceutix: The shorter continues to intentionally mislead readers by discussing gram-negative infections and brilacidin. Brilacidin is active against Gram-positive and is active against some, but not all, Gram-negative bacteria. Based on its activity profile, ABSSSI was selected as the target indication since organisms associated with these types of skin infections (Gram-positive S. aureus and Group A Streptococcus species) are susceptible to brilacidin. Brilacidin is not designed to treat the Gram-negative organisms of Acinetobacter baumannii and Pseudomonas aeruginosa. Importantly these are not ABSSSI pathogens. In fact, the most successful drugs currently used to treat ABSSSI, (namely vancomycin, daptomycin and linezolid) are agents that are effective only against Gram-positive pathogens and are not active against any Gram-negative organism including Acinetobacter baumannii and Pseudomonas aeruginosa.

Shorter: EBSL Enterobacteriaceae is a gram-negative bacterium, which can acquire AMP (antimicrobial peptitde) resistance by several mechanisms, including by modulating the net negative charge of cell surface membrane and losing electrostatic affinity towards cationic AMP that leads to repulsion of Brilacidin away from the bacteria. This means that the bacteria adapt to, and rejects, the antiobiotic. This is why it is so difficult to treat.

Cellceutix: NOT RELEVANT and misleading. The eight bacteria listed above are all Gram-negatives. Brilacidin is not designed for use against Gram-negatives. Therefore, these eight bacteria were NOT targeted in the phase 2 trial. Brilacidin is for use against Gram-positives, such as Staph and Strep -- the organisms that typically cause skin infections.

Shorter: Similar AMP resistance is common in Staphylococcal species and Candida, which also possess certain structural features to avoid AMP interaction with the bacterial outer membrane and by reducing the net energy release to lower net negative charge in the cell wall.

Cellceutix: NOT RELEVANT -- Brilacidin is not being developed to treat Candida infections. Furthermore, stringent laboratory tests have been conducted to evaluate the emergence of resistance to brilacidin in S. aureus. The resistance frequencies are extremely low (<10^-11) and are lower than other commonly used antibiotics including daptomycin. In other types of resistance assays (serial passage) the emergence of resistance was not detected with brilacidin but was readily evident with daptomycin. These results have been reported at numerous scientific meetings and validate the premise that agents which act like brilacidin show a lower potential for resistance development. Results on mechanism of action studies (see below) also show that bacteria do mount resistance mechanisms similar to those seen for antimicrobial peptides but they are abortive and not effective, likely due to the unique molecular structure of the compounds (not peptides) and their rapid killing activity. Importantly, the claim has never been that resistance will not develop to brilacidin but rather brilacidin exhibits a lower probability for resistance development than other antibiotics, a claim that is supported by experimental data.

Shorter: Polymedix has reported anti-microbial efficacy of two Brilacidin-like compounds against Candida albicans and other fungal species. However, the results were based on controlled laboratory conditions which cannot be replicated in the human clinical trials due to drug resistance mechanisms of Candida.

As pointed out by the research studies, these fungal organisms can remain unscathed due to its ability to increase the drug efflux pumps -- which is something like the bacteria spitting out the ingested drug particles based on charge repulsion mechanisms induced by certain genes. Efflux pump-based resistance is also reported in gram-negative bacteria such as Neisseria gonorrhea and Yersinia.

If oral fungus and bacteria can resist Brilacidin via these mechanisms, we can presume Brilacidin as well as Brilacidin oral rinse are not useful for patients. Why? Real-world conditions are a lot messier than clinical lab conditions, and the drug already doesn't work in the most ideal conditions possible!

Cellceutix: NOT TRUE

The article states: "AMPs represent one of the most promising future strategies for combating infections and microbial drug resistance". By deduction, this includes the development of AMP-mimics, which have benefits over native AMP.
The potential negative aspects of AMPSs are not expected to occur, because Cellceutix has created fully synthetic small molecule mimics of host defense proteins, such as AMPs. These are termed "defensin-mimetics". These drugs are NOT the naturally occurring biological compounds (AMPs) cited in the article; instead, these are synthetic mimics of those compounds. Thus, they are specifically designed to have the positive properties of AMPs without the negative properties.
The shorter confuses fungal resistance with bacterial resistance, and hence, fungi with bacteria. Given the difference in these life forms and their resistance mechanisms, compounds are typically developed independently for bacteria and fungi.
The defensin-mimetics have already demonstrated a minimal propensity for the development of resistance in the laboratory through a variety of testing procedures designed to predict clinical resistance. However, like any antibiotic, one does not know the extent to which resistance could develop until the drug has been used in a large patient population, usually over several years of exposure. Nevertheless, compared to other early stage antibiotics, brilacidin has all the attributes that are consistent with reduced development of resistance, such as a) mechanism of action that does not favor survival and evolution of the bacteria; b) laboratory-documented low mutation frequencies; c) positive results from serial passage studies; d) stationary phase active, so that persistent bacteria can be destroyed before they become resistant bacteria. Moreover, the ability to give a single-dose, rather than multiple doses, removes patient non-compliance as a driver for resistance.
The shorter confuses the oral formulation of brilacidin as an antibacterial or antifungal formulation. While these microbes may be affected by brilacidin when instilled in the oral cavity, the oral rinse invokes the unique anti-inflammatory properties of the compound, which is the purported mechanism by which brilacidin can prevent and control oral mucositis in cancer patients.

Shorter: Disease-causing fungus possesses the ability to increase the level of protein-degrading chemical substances (enzymes) to inactivate any harmful foreign substances, including Brilacidin. Over decades, biopharmaceutical companies have been trying to reduce the proteolytic degradation by adding non-standard amino acids or by restricting the use of peptides. Despite these attempts by some of the biggest pharma companies in the world, who have real scientists working there and not people who fake their credentials, a viable antibiotic has remained elusive. While it is has been hoped that bacteria would not develop resistance against AMP, research studies have been reporting acquired resistance mechanisms of several bacterial strains and Candida spps, particularly against cationic AMP.

Cellceutix: NOT TRUE -- See above and below

Again, the shorter confuses biological proteins, such as AMPs, with fully synthetic mimics of those proteins. The whole point of mimicking the proteins is to retain the positive qualities and minimize (or eliminate) the negative qualities.
Again, the shorter confuses fungi and bacteria.
The term "resistance against AMP" is not the same as "antibiotic resistance". In the case of a synthetic antibiotic, such as brilacidin, "antibiotic resistance" is the relevant term. Brilacidin is not an AMP -- it is a synthetic mimic of an AMP.
Brilacidin is not being developed to treat Gram-negative and fungal infections. However, other brilacidin-related compounds have been shown to be active against a variety of Candida species and two articles describing these results have been published in highly respected peer reviewed journals (Ryan et al. 2014. Activity of Potent and selective Host Defense Peptide Mimetics in Mouse models of Oral Candidiasis. Antimicrob. Agents Chemother. 58:3820-3827; Hua et al. 2010). Activity of antimicrobial peptide mimetics in the oral cavity: I. Activity against biofilms of Candida albicans. Mol. Oral Microbiol. 25: 418-425). Furthermore, robust activity was evident in an animal model of oral fungal infection (well outside the "controlled laboratory conditions") and the compounds were active against drug-resistant Candida species and demonstrated low resistance potential, as seen for bacteria.

Shorter: Contrary to Cellceutix's claim that development of resistance against AMP is unlikely, it has been suggested that microbial resistance against AMP is still possible, according to a research study published by Peschel A & Sahl HG (2006).

As nature's gift, pathogenic microbes resist AMP by employing a variety of mechanisms for survival in the host. These include passive (constitutive mechanisms) and acquired (adaptive) resistance mechanisms in response to a stress or AMP.

Cellceutix: While resistance, in theory, could occur with any antimicrobial compound, the shorter's linked abstract provides no data to support the hypothesis on cationic AMP resistance. Even if it did provide the data, it would not be relevant to the shorter's argument. This is because the defensin-mimetics, as stated previously, are not active biological proteins, like AMPs -- instead, they are synthetic mimics of AMPs.

Shorter: A study by Manniello et al has suggested that disruption of the outer membrane layer was not itself sufficient to render the pathogen susceptible to antimicrobial peptides. Here, you should note that the prime mechanism of action of Brilacidin is by disruption of the bacterial outer membrane layer.

Cellceutix: Besides disrupting the membrane, brilacidin also works by inducing misfolding of cytoplasmic protein. More importantly, the linked article describes a study on Pseudomonas, a difficult-to-treat Gram-negative bacteria. As noted above, brilacidin is not designed for use against Gram-negative bacteria.

The mechanism of action of brilacidin and other mimics has been studied extensively and two articles reporting the results have been published in a highly respected peer-reviewed journal (Mensa et al. 2014. Comparative mechanistic studies of brilacidin, daptomycin and antimicrobial peptide LL16. Antimicrob. Agents Chemother. 58: 5136-45; Mensa et al. 2011. Antibacterial Mechanism of Action of Arylamide Foldamers. Antimicrob. Agents Chemother. 55: 5043-5053). The results show that the compounds attack both the outer and inner membrane of Gram-negative bacteria and the inner membrane of Gram-positive bacteria (which lack an outer membrane) and disrupt barrier functions and membrane-associated metabolic processes leading to rapid bacterial death. Furthermore, as stated above, results from these studies show that bacteria do mount resistance mechanisms similar to those seen for antimicrobial peptides but they are abortive and not effective against brilacidin and related mimics, likely due to the unique molecular structure of the compounds (not peptides) and their rapid killing activity.

Shorter: Some gram-negative bacteria, including Pseudomonas and S. aureus, can effectively use certain chemicals to reduce the net (negative) charge of cell membrane to escape from AMP action. On the other hand, they can manage to create more positive charge in the outer cell wall, by which they can repel the positively-charged Brilacidin.

Simple physics -- Same charges repel and opposite charges attract! These superbug bacteria are often adaptive.
Cellceutix: NOT TRUE

As above, Brilacidin is not designed for use against Psuedomonas or other Gram-negative bacteria.
Stapylococcus aureus is NOT a Gram-negative organism. It is a Gram-positive organism. Multiple studies (in test tubes, in animals, and in people) have confirmed brilacidin's activity against Gram-positive organisms such as Stapylococcus aureus, including methicillin-resistant strains (MRSA).

Shorter: Apart from these AMP resistance mechanisms, gram-negative bacteria, including S. aureus, evade AMP attack by limiting the body functions, as well as the net energy (positive charge) release, which is the end-product of energy synthesis. S. aureus can elicit drug resistance by hiding deep inside the complex body (cell) structures, such as interior environment of blood vessel cells, where AMPs cannot reach. Pseudomonas aeruginosa escapes AMP action by hiding inside certain body cells, such as kidney, heart and spleen cells, which possess abnormally high positive charges. Certain bacteria, like Hemophilus influenza (flu-causing bacteria), can produce chemically varied cell wall chemicals that are deterrent to AMP attack. Pseudomonas fluorescens can replace the positive charge bacterial cell wall chemicals with negatively-charged cell wall chemicals to elicit drug resistance.

Unlike humans, environmental stress (exposure to AMP) can help the bacteria to evolve and adapt to extreme situations by activation of certain genes (PhoP/PhoQ regulon gene) which can aid the bacterial survival by altering/changing the chemical nature of the bacterial cell wall and cause AMP resistance.

Cellceutix: Similar responses were observed in the mechanism of action studies described above and shown to be ineffective against brilacidin and other mimics.

These genes are also involved in the release of protein-degrading chemicals that can even digest Brilacidin.

Cellceutix: Brilacidin is not a peptide and is not susceptible to protein degrading enzymes.

Shorter: These genes are commonly present in S. aureus and E. coli. The notable point is that Cellceutix has tested and reported that Brilacidin was effective against these two bacteria.

Cellceutix: Correct, but limited against E. coli, a gram-negative bacteria.

Shorter: Unlike humans, environmental stress (exposure to AMP) can help the bacteria to evolve and adapt to extreme situations by activation of certain genes(PhoP/PhoQ regulon gene) which can aid the bacterial survival by altering/changing the chemical nature of the bacterial cell wall and cause AMP resistance. These genes are also involved in the release of protein-degrading chemicals that can even digest Brilacidin. These genes are commonly present in S. aureus and E. coli. The notable point is that Cellceutix has tested and reported that Brilacidin was effective against these two bacteria.

Cellceutix: NOT TRUE

Stapylococcus aureus is NOT a Gram-negative organism. It is a Gram-positive organism.
Haemophilus influenzae is a bacteria. It does NOT cause the "flu". Influenza (the "flu") is caused by the Influenza viruses.
Brilacidin is not active against Gram-negative bacteria, such as Pseudomonas. It was never intended to be used for Pseudomonas infections.
"Protein-degrading chemicals" are not relevant because brilacidin is NOT a protein. Instead, it is a synthetic mimic of proteins, such as AMP. This is one of the reasons the defensin -- mimetics were developed -- to avoid protein degradation.
Yes, multiple studies (in test tubes, in animals, and in people) have confirmed brilacidin's activity against Gram-positive organisms such as Stapylococcus aureus, including methicillin-resistant strains (MRSA). Neither the FDA, nor Institutional Review Boards (IRBs), would allow this drug to be used to treat serious Staph aureus infections in human beings unless there were data to support its activity. http://cellceutix.com/brilacidin/#sthash.eaZNIUrn.dpbs and http://cellceutix.com/wp-content/uploads/2013/11/A-Randomized-Double-Blind-Study-Comparing-Single-Dose-and-Short-Course-Brilacidin-to-Daptomycin-in-the-Treatment-of-Acute-Bacterial-Skin-Skin-Structure-Infections-ABSSSI1.pdf

Shorter: One of the key tenets of the bull case on CTIX is that Brilacidin is supposedly effective against A. baumannii bacteria. It is not.

Cellceutix: NOT RELEVANT

Shorter: Out of four organisms that make up the so-called superbugs that resist antibiotic treatment, A. baumannii is a pleomorphic and gram-variable organism -- meaning, it can change itself into either a gram-positive or gram-negative organism. Treating A. baumannii infection is a challenging task, and hence, focusing on prevention rather than treatment is a wise option.

It is not viable to expect Brilacidin's efficacy against A. baumannii, as the AMP failed to prove its efficacy against all bacteria. A. baumannii is a common causative of hospital-borne infections. Even Cellceutix has accepted that Brilacidin is ineffective against A. baumannii. The treatment inefficacy is generally due to release of a proteolytic mechanism, over-expression of drug efflux pumps, and changing the structure and function of certain molecules to which the antibiotic binds and acts.

Cellceutix: NOT RELEVANT

A. baumannii is a Gram-negative bacteria. It is not a common cause of skin infections. Brilacidin was not developed for the treatment of Gram-negative infections, such as A. baumannii. It was specifically developed for the treatment of Gram-positive infections, such as acute bacterial skin and skin structure infections (ABSSSI) caused by Staphylococcus aureus, including methicillin-resistant strains (MRSA). Brilacidin is not active against A. baumannii and other Gram-negative organisms due to differences in membrane composition between susceptible (Gram-positive) and non-susceptible organisms. Efflux responses and protease degradation are not responsible for differences in susceptibility. Other mimics have been identified that are active against Gram-negative organisms due to structural differences between these compounds and brilacidin.

In addition, "Protein-degrading chemicals" and "proteolytic mechanisms" are not relevant because brilacidin is NOT a protein. Instead, it is a synthetic mimic of proteins, such as AMP. This is one of the reasons the defensin -- mimetics were developed -- to avoid protein degradation.

Shorter: All these disease-causing bacteria, including S. aureus, Pseudomonas, and E. coli, have been tested by Cellceutix to prove Brilacidin's efficacy. It is now clear for us that the drug is not effective any of the infectious bacteria that cause serious, life-threatening problems in a clinical care setting.

Cellceutix: NOT TRUE -- for reasons given above.

Although the shorter mentions the importance of a "clinical care setting, very few of the their references cite data collected in a "clinical care setting". Most are laboratory studies, in vitro or in animals.

It is important to review clinical data, when available. Cellceutix has positive clinical data -- data derived from real human beings treated for their infections. FDA approval rests upon a rigorous clinical trial process on a pre-specified number of human patients.

Shorter: According to research studies, like gram-negative bacteria, gram-positive bacteria, including Pseudomonas aeruginosa (note P. aeruginosa is Gram-negative), Enterococcus fecalis and Mycobacterium tuberculosis (TB bacteria), possess drug resistance mechanism by reducing net negative charge in the outer membrane to repel all positive charged molecules that comes into contact, including Brilacidin. According to the same study, Cellceutix has claimed that Brilacidin, a cationic AMP, is highly effective against these three microbial pathogens -- which seem to be a blatant false, as per our above review.

Cellceutix: NOT TRUE

Brilacidin is engaged in a gram-positive clinical study. It was never intended to be used for Gram-negative infections or mycobacterial infections.

Shorter: Despite this scientific rationale, the company has been maintaining that Brilacidin is effective against gram-negative bacteria, and incidence of resistance is "unlikely" - which seems to be joke.

Cellceutix: Brilacidin is engaged in a gram- positive clinical study. Brilacidin is not active against some Gram-negative bacteria, such as Pseudomonas. It was never intended to be used for Gram-negative infections or mycobacterial infections.

Brilacidin has the potential to minimize the development of resistance, for reasons given above.

Shorter: Cellceutix is currently evaluating the safety and potential of Brilacidin in a Phase II trial against oral mucositits in cancer (head and neck) patients. Oral mucositis usually gets worse if it gets infected. The aim of Brilacidin treatment is to prevent infection, by which it may reduce/improve mouth and throat soreness and improve the quality of life.

Cellceutix: Brilacidin has demonstrated robust activity in stringent animal models of oral mucositis that are susceptible to secondary bacterial or fungal infections. Results from these studies have been presented at several scientific meetings and slides summarizing this activity are linked below.

Shorter: Our review on the "science" of Brilacidicin has contradicted the claimed benefits, especially the antimicrobial activity. Hence, the efficacy and safety of Brilacidin oral rinse are now questionable.

Cellceutix: NOT TRUE

While patients with oral mucositis are at risk of infection through open ulcers, the disease is not caused by infection. Accordingly, brilacidin's efficacy in oral mucositis is not based on its antibiotic properties. Rather, it is based on its immunomodulatory properties. Indeed, positive data from reliable animal models of oral mucositis (without evidence of concomitant bacterial infection) support an immunomodulatory, rather than antimicrobial, mechanism of action.

Thus, for oral mucositis, the shorter's claim that "the aim of Brilacidin treatment is to prevent infection" is false.

http://cellceutix.com/brilacidin-om/#sthash.NXoI4DwG.dpbs

http://cellceutix.com/wp-content/uploads/2013/11/ECCMID-2015-OM-poster.pdf

https://clinicaltrials.gov/ct2/show/NCT02324335?term=cellceutix&rank=2

Shorter: The company has cleverly pitched the safety and efficacy data of Kevetrin to investors without publishing the results in medical journals. Is this designed to keep investors and the public in the dark, without disclosing the "real" efficacy and safety of the drug?

Cellceutix: Kevetrin is still in a Phase 1 trial. Results will be published in a medical journal at the study's conclusion, as is customary to Phase 1 trials.

Shorter: If we take a closer look into the reported mechanism of action, we've got several doubts about the possible inefficacy and rationality of Kevetrin use as a cancer treatment, as it acts by targeting only one molecule: p53.

Cellceutix: p53 is the most frequently altered gene in human cancer (http://www.nature.com/scitable/topicpage/p53-the-most-frequently-altered-gene-in-14192717 ), so to downplay the importance of targeting the protein dubbed the "Guardian Angel" of the human genome, makes no logical sense.

Shorter: Summary of key points

Kevetrin has no direct action on cancer cells.

Cellceutix: Kevetrin has significant activity on cancer cells and all studies show otherwise. http://cellceutix.com/kevetrin/#sthash.mJm107rx.dpbs
Kevetrin received FDA Orphan Drug Designation for a cancer indication. Proof of efficacy was provided in the submitted application.

It may target cancer cells, but not cancer stem cells, which is very important for anti-cancer

treatment.

Cellceutix: There is no drug approved for targeting cancer stem cells. We have never made this claim as no such experiments were conducted. Hence, the shorter is drawing a conclusion on his own without any scientific evidence. Further, the concept of cancer stem cells has only been recently introduced in the scientific community and is still in early phase of investigation.

Keventrin's reported benefits were based on an invalid endpoint, p21, as a biomarker.

Cellceutix: The clinical trial design was a collaborative effort between Cellceutix and the world-class oncology experts at Harvard's Dana-Farber Cancer Institute, the host of the clinical trial. Calling p21 an invalid endpoint is inaccurate. p21 is a biomarker for p53 activation that we are measuring in the peripheral blood of patients, not in the tumor tissue. p21 is a downstream gene in the p53 signaling activation pathway. Therefore enhancement in p21 gene expression is the indication of p53 activation in peripheral blood cells.
http://www.ncbi.nlm.nih.gov/pubmed/?term=Tumor+Susceptibility+of+p21Waf1%2FCip1-deficient+Mice1

Cellceutix has made misleading claims about cancer regression from patients who discontinued the trial.

Cellceutix: Phase 1 stipulates to identify the maximum tolerated dose (MTD), PK, adverse effects. All reported cases of benefit were observed and recorded by the clinical team. Cellceutix disclosed the near complete disappearance of a metastatic lesion in the spleen of a Stage 4 ovarian cancer patient who successfully completed three cycles of Kevetrin. To say Cellceutix made misleading claims is completely false. As explained in the press release ( http://cellceutix.com/cellceutix-reports-spleen-lesion-disappears-in-patient-with-metastatic-stage-4-ovarian-cancer-in-clinical-trial-of-anti-cancer-drug-kevetrin/#sthash.AF3fDz2M.dpbs ), the patient's CA125 count was elevated (a common occurrence in cancer patients) and she was advised to discontinue the trial by her physician; Cellceutix was provided no further information on rationale behind the decision.

Shorter: Cellceutix has claimed that Kevetrin treatment can activate the wild-type p53 (normal, without mutational changes), as well as mutated p53, which seems to be a tall claim.

Cellceutix: Cellceutix has published information and presented posters at leading oncology conferences on the mechanism of action of Kevetrin regarding wild-type and mutated p53.
http://cellceutix.com/wp-content/uploads/2014/06/A-phase-1-dose-escalation-safety-pharmacokinetic-pharmacodynamic-study-of-thioureidobutyronitrile-a-novel-p53-targeted-therapy-in-patients-with-advanced-solid-tumors..pdf
http://cellceutix.com/about-kevetrin/#sthash.72PfU9Ax.dpbs
http://cellceutix.com/wp-content/uploads/2014/06/Cellceutix-Slide-Deck-BioTech-Showcase-12-Jan-2015-B-2.pdf

Shorter: If we look into the molecular basis of cancer, it is impossible to activate the wild-type p53 without inhibiting the release of MDMX and MDM2 proteins, which are the natural inhibitors of p53. Meaning, these two molecules naturally inhibit p53 expression in the cells. Kevetrin just acts on p53, but not on MDMX and MDM2, which can lead to persistent inhibition and unavailability of wild-type p53. So, it is important to target MDMX and MDM2 proteins prior to Kevetrin treatment to achieve complete treatment benefits.

Cellceutix: Not True. Cellceutix has reported phosphorylation of MDM2, included in a presentation at an American Association for Cancer Research meeting. http://cellceutix.com/wp-content/uploads/pdfs/AACR%20poster2012MAR29%2011x17%20FINAL.pdf

Shorter: If Kevetrin can prevent cancer development by curbing abnormal cell multiplication and by maintaining a normal cell cycle, what will the effect be on already developed cancer cells? Maybe Cellceutix's answer is -- induction of "cell-suicide" in cancer cells. In reality, cancer cells can evade almost all the anti-cancer mechanisms, including programmed cell death (apoptosis), and remain immortal.

Cellceutix: No such claims were made and no such studies were conducted regarding cell cycle effects.

Kevetrin induces apoptosis by PARP cleavage. The shorter does not have adequate knowledge of basic molecular biology and cancer therapies. Standard cancer treatment regimens involve intervening in multiple molecular pathways.

Shorter: You may wonder why cancer treatments often fail, despite much advancement in science and technology. It is because almost all anti-cancer drugs either target the cancer cells or the cancer-causing genes, like p53. In a tumor, the cancer cells are unlimitedly supplied by cancer stem cells, which is the root cause of the problem. Cancer stem cells are present inside the tumor itself. Any anti-cancer treatment will fail if these cancer stem cells remain untouched. Clearly, Keventrin is not a panacea for cancer treatment and is no superior than other anti-cancer drug, because it cannot eliminate cancer stem cells effectively.

Cellceutix: As mentioned above, no testing has ever done with Kevetrin on cancer stem cells, so there is no basis to say whether it does or does not. I'm certain the shorter knows but didn't say that there is no existing approved drug that address cancer stem cells.

Shorter: If Kevetrin can degrade mutant p53, what is the mechanism of action? The activation of p53 is via a different pathway. It doesn't make sense. Mutant p53 degradation involves several chemical (enzymatic) and genetic (molecular biological) reaction/mechanisms, such as caspase-induced mechanisms and both transcriptional-dependent and transcriptional-independent pathways. The company has not disclosed Kevetrin's exact mechanism of action on mutant p53.

Cellceutix: Please refer to link for proteasomal degradation by Kevetrin. It was presented at American Society of Clinical Oncology Meeting 2013. http://cellceutix.com/wp-content/uploads/2012/07/ASCO-poster-Kevetrin-2013-JUN-03-FINAL.pdf

Shorter: To overcome these clinical problems, Kevetrin should be tested alongside other medications, including conventional anti-cancer drugs, to see the potential drug interactions. But in the clinical trials, Cellceutix has not co-administered any other drugs.

Cellceutix: In a Phase 1 trial you cannot combine drugs. The goal of a Phase 1 is to determine the MTD and to see the toxicity of the drug. Thus it cannot be combined. The shorter is stating something that, besides not making sense, is not possible for any drug and would not be allowed by the FDA.

Shorter: Certain cancer patients have tumors without wild-type p53 and with defective genetic makeup in p53 with the presence of only one functional allele (variant of the gene) instead of two. In addition, some patients can lack certain regions of the gene or have other p53 gene variants, such as p.S106R. The binding mechanism of Kevetrin with p53 cannot work with these defective variants, due to structural variations. Cellceutix has not considered these limitations, as most of the reported benefits were based on animal studies, not in humans.

Cellceutix: This is the unique advantage of Kevetrin where it can act on wild type p53, even if there is 1 mutant allele.

Shorter: In Phase II clinical trials, Cellceutix has claimed that the tumors were eliminated (regressed) in Kevetrin-treated ovarian cancer patients. But the study has not followed up with the patient to report whether the regression was complete or partial or had appeared again (relapse). Cleverly, the company has evaded these questions by announcing that the patient has discontinued the trial. It doesn't make sense - if the treatment is really effective, what made the patient discontinue the treatment? Why would you announce positive results if the patient discontinued? Is this just part of the stock promotion?

Cellceutix: Kevetrin is not in a Phase 2 trial. The Phase 1 trial is to test Kevetrin against a wide range of solid tumors, which includes ovarian cancers. Again, the press release (linked above) explained the situation with the ovarian cancer patient clearly.

Shorter: p21: An invalid biomarker -- Why did Cellceutix choose this?
Cancer is a multi-factorial disease, and p53 is not the only molecule involved in the onset of the disease. Survivin is an independent and important protein (biomarker) involved in key pathways of p53 regulation (release and inhibition). Why has Cellceutix not considered Survivin as a potential biomarker to evaluate the prognosis and treatment benefits of Kevetrin? Seems questionable!

Cellceutix: The shorter provides a link to a potential marker to ovarian cancer. However the trial title is A Safety, Pharmacokinetic and Pharmacodynamic Study of Kevetrin in Patients With Advanced Solid Tumors (https://clinicaltrials.gov/ct2/show/NCT01664000?term=cellceutix&rank=4 ). The shorter seems to be trying to confuse readers to think that Cellceutix is conducting a trial on ovarian cancer specifically. The biomarker we use for measuring p53 activity is p21. This was in consultation with Harvard's Dana-Farber Cancer Institute conducting the study and is the gold standard. http://www.ncbi.nlm.nih.gov/pubmed/?term=Unravelling+mechanisms+of+p53%E2%80%91mediated+tumour+suppression
http://www.ncbi.nlm.nih.gov/pubmed/?term=The+MDM2-inhibitor+Nutlin-3+synergizes+with+cisplatin+to+induce+p53+dependent+tumor+cell+apoptosis+in+non-small+cell+lung+cancer

Shorter: According to Cellceutix, in the stage-4 ovarian cancer patient who was clinically stabilized, increased level of CA-125 count was observed in the third month. An elevated level of CA-125 suggests the ongoing risk of cancer development, ineffective treatment and worse survival chances.

Cellceutix has cleverly employed an invalid biomarker instead of a reliable one for cancer. Recent research results have discarded p21 in cancer studies, citing that p21 is a NOT a valid biomarker for ovarian cancer prognosis or to assess the treatment benefits.

Cellceutix: Again the shorter is confused thinking we are now doing an ovarian cancer trial, which the link specifically addresses. Even if that were the case, there are different areas of sampling (i.e tumor, peripheral blood, etc.). The article and the shorters statement makes no sense and misleads readers to believing we are in an ovarian cancer trial.

Shorter: However, p53 is still reliable -- which Cellceutix has not examined in the trial subjects, as the company didn't consider p53 as a biomarker of ovarian cancer assessment.

Cellceutix: This is exactly what we are doing with p21.

Shorter: This is dubious. p53 analysis can be done overnight in any laboratory, and may cost about a few hundred dollars. This is a basic test. Why did Cellceutix not pursue this?

Cellceutix: The shorter does not understand Phase 1 clinical trial protocols. It is not an acceptable practice, nor would any hospital allow numerous tumor biopsies to be taken from Stage IV cancer patients. Therefore we use p21.

Shorter: An independent Swedish study has reported that about 19% of ovarian cancer patients with p21 NEGATIVITY and positive p53 had a poor survival outlook. In the same study, about 9% of ovarian cancer patients (with non-serous type tumors) with CONCOMITANT p21 and p27 positivity had EXCELLENT SURVIVAL OUTLOOK.

Based on the review of these research studies, it is now clear that p21 is not a valid or reliable biomarker to predict ovarian cancer treatment benefits.

Cellceutix: Again this is not an ovarian cancer trial. The shorter apparently does not understand the Swedish paper.

Shorter: What baffled us was, despite this irrefutable research support, why has Cellceutix not considered this invalid biomarker as a secondary endpoint?

Cellceutix: What baffled us is the shorter has no clue of our Phase 1 trial but continues to make such statements.

Shorter: Cellceutix's anti-psoriatic pipeline candidate, Prurisol, is a chemically modified version (esterified) of already approved anti-HIV drug Abacavir. Once again, the company has not disclosed the exact nature of modification (peptide or amino acid modification).

Cellceutix: This information is in the Patent for Prurisol that is publicly available in Google Patents.

Shorter: Abacavir has more side effects and fewer benefits: the antiviral drug causes serious allergic reactions, and increases the risk of heart diseases in treated patients. The structure of Prurisol mimics three drugs, such as Methotrexate, Abacavir and Cladiribine.

Cellceutix: The shorter contradicted himself by first stating we have not disclosed the structure, now he compares the structure to other drugs.

Shorter: Summary of key points for prurisol

Prurisol treatment can cause very serious side effects.

Cellceutix: The trials exclusion criteria are in place to avoid any ill effects.

All reported benefits were based on animal studies conducted by KARD Scientific, which is a research institute owned by Menon.

The availability of proven anti-psoriatic drugs can boot out Prurisol from the market.

Cellceutix: Most effective anti-psoriatic drugs are biologicals. Because of that, the adverse effects are very high. Prurisol is an orally bioavailable small molecule.

Shorter: As reported by Cellceutix, Prurisol is an inactive form (prodrug) of Abacavir with undisclosed structural modifications to act against certain immune proteins (Interleukin-20; IL-20) that cause worsening of psoriasis symptoms. The company has modified Abacavir to bypass intestinal secretion-induced loss of drug. In animal studies, Prurisol has reduced the presence of certain genes (PRISM) (Cellceutix: shorter again shows his lack of knowledge as it is "PRINS") and immune proteins that are associated with inflammation (IL-20, CD-4 and CD-8).

Cellceutix: The shorter also has no understanding of immunology. CD-4 and CD-8 are not inflammatory proteins, they are T cell markers. http://www.ncbi.nlm.nih.gov/pubmed/1909592

Shorter: In early studies, Cellceutix has validated the similarities (chemical and mechanism) of Prurisol and Abacavir in healthy subjects. The company just initiated a Phase II, trial and patient enrollment is still on. Prurisol has a long way to go to prove the safety and efficacy. Even if it passes through the clinical trials, the availability of already proven anti-psoriatic drugs (TNF alpha inhibitor drugs) can threaten the commercial success of Prurisol.

Cellceutix: These are all biologicals and side effects can be severe that in many cases treatment has to be stopped.

Cellceutix: The shorter continues with attempted character attacks. He references an article that once appeared in a publication named INDIA New England. The article was as ridiculous as the one written by the shorter. After presenting the publisher with proof he quickly removed the article and all links to it.

We thank our shareholders for their continued participation and support in our goal to make Cellceutix one of the really great biotech success stories.

Sign-up for Cellceutix email alerts is available at http://cellceutix.com/email-alerts/#sthash.CRfqSmmY.dpbs

About Cellceutix:
Headquartered in Beverly, Massachusetts, Cellceutix is a publicly traded company under the symbol "CTIX". Cellceutix is a clinical stage biopharmaceutical company developing innovative therapies in oncology, dermatology and antimicrobial applications. Cellceutix believes it has a world-class portfolio of compounds and is now engaged in advancing its compounds and seeking strategic partnerships. Cellceutix's anti-cancer drug Kevetrin is currently in a Phase 1 clinical trial at Harvard Cancer Centers' Dana Farber Cancer Institute and Beth Israel Deaconess Medical Center. In the laboratory Kevetrin has shown to induce activation of p53, often referred to as the "Guardian Angel Gene" due to its crucial role in controlling cell mutations. Cellceutix is in a Phase 2 clinical trial with its novel compound Brilacidin-OM for the prevention of Oral Mucositis in patients with head and neck cancer. Brilacidin-OM, a defensin mimetic compound, has shown in an animal model to reduce the occurrence of severe ulcerative oral mucositis by more than 94% compared to placebo. Cellceutix's anti-psoriasis drug Prurisol is in a Phase 2 trial. Prurisol is a small molecule that acts through immune modulation and PRINS reduction. Cellceutix's lead antibiotic, Brilacidin, has completed a Phase 2b trial for Acute Bacterial Skin and Skin Structure Infections, or ABSSSI. Top-line data have shown a single dose of Brilacidin to deliver comparable clinical outcomes to the FDA-approved seven-day dosing regimen of daptomycin. Brilacidin has the potential to be a single-dose therapy for certain multi-drug resistant bacteria (Superbugs). Cellceutix has formed research collaborations with world-renowned research institutions in the United States and Europe, including MD Anderson Cancer Center, Beth Israel Deaconess Medical Center, and the University of Bologna. More information is available on the Cellceutix web site at www.cellceutix.com.

Forward-Looking Statements
This press release contains forward-looking statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995 that involve risks, uncertainties and assumptions that could cause Cellceutix's actual results and experience to differ materially from anticipated results and expectations expressed in these forward looking statements. Cellceutix has in some cases identified forward-looking statements by using words such as "anticipates," "believes," "hopes," "estimates," "looks," "expects," "plans," "intends," "goal," "potential," "may," "suggest," and similar expressions. Among other factors that could cause actual results to differ materially from those expressed in forward-looking statements are Cellceutix's need for, and the availability of, substantial capital in the future to fund its operations and research and development; including the amount and timing of the sale of shares of common stock to Aspire Capital; the fact that Cellceutix's compounds may not successfully complete pre-clinical or clinical testing, or be granted regulatory approval to be sold and marketed in the United States or elsewhere. A more complete description of these risk factors is included in Cellceutix's filings with the Securities and Exchange Commission. You should not place undue reliance on any forward-looking statements. Cellceutix undertakes no obligation to release publicly the results of any revisions to any such forward-looking statements that may be made to reflect events or circumstances after the date of this press release or to reflect the occurrence of unanticipated events, except as required by applicable law or regulation.

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Contact Information:

INVESTOR AND MEDIA CONTACT:
Cellceutix Corporation
Leo Ehrlich