Big Pharma has a Shrinkage Problem

Big Pharma can't kill tumors. “We are pretty good at shrinking tumors, but not good at getting rid of them. Immune therapy is a way to begin to approach that.” -- Merck senior vice president Gary Gilliland (from an article by Robert Langreth on May 12, 2013)

I think most people would agree killing tumors should go a long way in fighting, arresting and perhaps even killing cancer. Medical literature discusses the positive correlation between complete response -- the tumor, after treatment, goes away -- and overall survival, "...the gold standard primary end point to evaluate the outcome of any drug, biologic, intervention, or procedure that is assessed in oncologic clinical trials."

Big Pharma is making process. Stabilizing the disease, by preventing the further growth of cancerous tumors, is good. Shrinking them is better.

Killing them is best.

While Big Pharma's oncology drugs and drug candidates are increasingly demonstrating better overall responses (or overall response rates), complete response plus partial response (shrinking the tumor), it's struggling to improve complete response (killing the tumor).

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And it doesn't look like Big Pharma will solve the problem of killing tumors -- achieve better complete responses -- anytime soon, because it appears pharmaceutical companies are hitting a ceiling for complete response.

From my November 23, 2013 post [We] now believe...[we] have sufficient information to seek regulatory approval: I read an interesting abstract at the 2013 Society for Immunotherapy of Cancer ("SITC") Annual Meeting, co-authored by Martin Ashdown and Provectus principal investigator Brendon Coventry: Mathematical modeling of immune kinetics in advanced cancer through meta-analyses of complete response rates: immune synchronisation emerges as the likely key determinant of clinical response. Ashdown et al.'s work comprised a meta-analysis of 130 clinical trials, 8,000 patients, different solid tumor cancers, and standard chemotherapy, targeted therapy and iimmunomodulatory therapy compounds IL-2, ipilimumab, tremelimumab, cytotoxic agents, TMZ, dabrafenib, vemurafenib, PD-1s (BMS, Merck) and a PDL-1 (Genentech).

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Ashdown and Conventry concluded:"Mathematical analyses of over 130 clinical trials, inclusive of over 8000 patients, has demonstrated that the CR rate for patients treated with widely divergent therapies is remarkably fixed at between 5 and 10%. The probability of this occurring by chance alone is extremely close to zero, and is both scientifically and clinically implausible. Therefore, an underlying predictive operative biological mechanism must apply. It is highly likely that the known principles of immune kinetics between effector and regulatory homeostatic functions must therefore determine a degree of immune synchronization to produce these observed CR’s. We have derived a mathematical model and equation using the principles of controlled homeostatic systems, which can be used to explain our meta-analysis findings, and the clinical efficacy." Bold and underlined emphasis is that of Ashdown et al. from their SITC poster presentation.