Pharma Strategy Blog

Commentary on Pharma & Biotech Oncology / Hematology New Product Development

Posts tagged ‘oncology’

Yesterday, I mentioned that some of the best bits of this year’s American Association for Cancer Research (AACR) meeting were the numerous gems in the poster sessions.

Reuben Sierra, Ming Tsao's Lab (with permission)

One of the coolest such posters I came across was from Ming Tsao’s group.

Specifically, Rafael Sierra (see photo right) was hosting an excellent piece of research entitled: Overcoming resistance to EGFR-tyrosine kinase inhibitor therapy in non-small cell lung cancer.

This is an area of much needed research and breakthroughs.

Why?

Well, at the ECCO meeting in Stockholm last September, Tom Lynch was discussing the role of one such EGFR therapy, cetuximab (Erbitux), in lung cancer and wearily declared prior to presenting a negative study,

“If ever there was a drug desperately needing a biomarker, it’s cetuximab”

because while some of the patients responded beautifully to the drug, many others didn’t and at that time, there was no way to determine upfront who might respond before treating.

This is clearly a waste of valuable resources and time because catch-all studies mean that the number of negative responses can balance out the positive responses in too heterogeneous a population.  That said, if you know what the potential target(s) or biomarker of response are, then you can select patients more precisely for a study and improve the subsequent overall response rates and OS advantage dramatically.

As Sierra et al., pointed out in their poster at AACR, we do know that:

“Patients that present amplification or activating mutations (L878R or exon 19 deletions) of EGFR, have higher response rates. Selection improved response rates from less than 10% to over 60–80%.”

This is very good progress, but how did their research take this concept further?

In this study, the group reported the preliminary findings from a complex study of genome-wide screenings on EGFR resistant cells to try and identify new genes that might mediate resistance and, importantly, be potentially druggable, unlike say, MYC. This would then offer new logical targets for combination therapies to be tested in the clinic in patients to determine if outcomes could be improved.

At the time of the poster presentation, the group had indeed identified a short list of potential candidates (not named as this would be available in a later publication). Conceptually though, this was an elegant study and I really liked the concept.

This morning, I was delighted to see a news snippet from the 3rd European Lung Cancer Conference in Geneva, Switzerland where the ESMO press release noted that Dr Tsao’s group performed:

“An exploratory analysis on the TORCH patient tumor samples that were available for analysis, looking for molecular biomarkers known to be potential predictors of benefit from EGFR inhibitors.”

Despite the biomarker analysis being pre-planned, however, only a third (36%) of samples were available for analysis. It is always harder to do retrospective mutation analysis on small sample sizes unless rigorously collected as per the BATTLE trials.

I’m looking forward to hearing what targets were identified in Drs Sierra and Ming’s research once published or presented in more detail at a future conference, as this may help us move the field forward in terms of rational combinations to either overcome resistance to EGFR therapy (other than the well known T790M mutation) or prevent resistance from developing early.

Now, that would be very cool and I do hope they alert us to the publication in due course – watch this space!

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This morning I was pondering a triangulation of several random thoughts that appeared in my Twitter stream, many from BIO, about various topics:

  1. Discussing the patent cliffs and lack of revenue generation some companies such as Lilly will no doubt be facing with John Carroll (Fierce Biotech) and Matt Herper (Forbes Health)
  2. Christiane True (PharmaLive) at the annual BIO meeting quoted a speaker as saying “doing more with less” which seems pretty much de rigeur these days
  3. Ron Leuty tweeted a quote from Chris Viehbacher’s (Sanofi) presentation at BIO, “Not doing more with less, but doing different things.”
  4. Christiane also quoted Viehbacher, “Still not enough of bright science making its way to patient benefit.”

The last point particularly made me wonder, because quite a few oncology companies have broad and deep pipelines, often with more compounds than they can possibly advance at once.  Even big Pharma or Biotech has to rationalise resources, budgets and people or nothing would get done.

How do those decisions get made?

Some are smart at life cycle management (GSK and Roche spring to mind), some think strategically about their portfolios, others get mired down in politics or – even worse – distracted by numerous committees focusing on what I call ‘fluffy puffy’ abstract things instead of moving the compounds rapidly through the pipeline to become safe and effective drugs that make a difference to patients lives.

The future of successful cancer drug development is likely going rest heavily on investment in basic science, molecular biomarkers and diagnostics, and novel-novel clinical trials that target multiple aberrations driving the disease.

Investors aren’t interested in any of these things, though; most just want a rapid or high return on their investment.  Spending less on R&D is much more in tune with their short term thinking:

Viebacher: If you sit down with investors, they clamor to stop spending on R&D, just do a buyback. #BIO2011

Tweet from Christiane True (PharmaLive) at BIO

The thing is, if pharma companies are going to rely on buying or licensing late stage compounds from Biotech, there is only so much small to medium Biotechs will be able to do going forward, because the future will mean more diagnostics and biomarkers, which are very expensive in cancer research, and in some cases, prohibitively so.  This will require closer, earlier collaboration with Academia and even different types of trials thanwe have been used to in the old chemotherapy world.

There are sometimes more challenges with clinical trial designs in small biotechs going from phase II to III, as Sanofi discovered with BiPar and iniparib and Novartis with Antisoma and ASA-404.  If we want to reduce the number of phase III failures, we have to get smarter about more iterative studies in phase II, better patient selection, incorporation of biomarkers, more logical combinations and yes, all of these will cost more dollars that will likely give investors insomnia.

Finding out more about the compound earlier will be the new name of the game – it is obviously better to abandon a weak agent on phase I or II than expensive phase III trials.

In the end, the companies who will win out in the long run are often those who think strategically, drive innovation, focus on science-based research, license earlier rather than later, invest in biomarker/diagnostic research, work in close knit cross-functional collaborative groups, avoid the twin pitfalls of bad karma and politics and ultimately ‘see’ things more clearly than the pack allows them to translate that into meaningful action.

It occurred to me that if you have to ask who the KOLs and experts are, then you have a long way to go and that doesn’t inspire confidence in the agent you’re developing.  If you have too much greed in the boardroom C-level that’s clearly going to hamper things as well, especially if they want to implement cuts down the line.  All of these myriad of factors surprisingly do matter when it comes to riding out patent cliffs and maintaining R&D momentum.

I should probably add ‘corporately ignore the short term investors for long term solid gains,’ but that would be a bit cheeky, perhaps 😉

Ultimately, what I would really like to see is less talk and more effective action:

A lot of talk about benefits and challenges with personalised healthcare but no mention of solutions #BIO2011

Tweet from Pieter Droppert in the Personalised Medicine session at BIO

I guess that’s why the American Association for Cancer Research (AACR) remains my favourite meeting in the annual conference calendar – at least Academic attendees are presenting data and discussing solutions in informal chats in corridors or poster sessions on how to address the practical issues of improving cancer research.  Inevitably, the smart companies are tapping into this resource and working alongside each other to unravel the complex mysteries.


There is a provocative article in this week’s New England Journal of Medicine asking whether the accelerated approval process should be used for more cancer drugs:

“The striking results of recent phase 1 trials of targeted cancer drugs have provoked serious discussion about shortening the road to drug approval.”

The main thrust of the argument was that it takes on average seven years from entering human trials to approval if phase III trials are included in the oncology drug development process.

“Of the 23 oncologic drugs given accelerated approval between 1993 and 2008, two were ultimately withdrawn from the U.S. market — gemtuzumab because of toxicity and gefitinib because of lack of efficacy.”

The author argues that:

“Phase 3 trials are expensive and time-consuming, usually taking at least 2 to 3 years to reach survival end points. The news of a highly successful new compound in phase 1 or 2 rapidly reaches physicians and patients, creating demand for early access.”

While we have seen some successes with the Accelerated Review process with imatinib (Gleevec), erlotinib (Tarceva), cetuximab (Erbitux), bevacizumab (Avastin) and others, there has also been a flood of promising phase II agents that duly flopped in randomised phase III trials, with Pfizer’s figitumumab, Novartis/Antisoma’s ASA404 and sanofi-aventis’ iniparib to name a few off the top of my head.

One of the challenges here is that companies often take a targeted therapy but strangely test it in an unselected patient population, which will increase the chances of failure in a more rigorous randomised phase III trial.  In an ideal world, several carefully designed adaptive phase II trials would help develop logical combinations and markers of response, thus increasing the chances of success in phase III studies.

The big problem as I see it then, is that while we have exciting new agents likely to be approved in 2011 such as:

  • crizotinib in lung cancer
  • ipilimumab (Yervoy) and PLX4032 (vemurafenib) in metastatic melanoma
  • brentuximab vedotin in Hodgkin Lymphoma
  • abiraterone acetate (Zytiga) in prostate cancer

we don’t always know how to carefully select patients to enable treatment based on the underlying molecular basis of the disease.

Of those mentioned above, with crizotinib (ALK), vemurafenib (V600E BRAF) and brentuximab (CD30) we clearly do, but with abiraterone and ipilimumab the issue of patient selection seems less clear at the moment.  Sadly there are not any biomarkers available to tell us which patients are most likely to benefit from treatment in targeted therapies already approved such as bevacizumab.

The fate of bevacizumab in breast cancer has yet to be determined.  It was approved under the FDA Accelerated Review process based on the initial phase II data, with the assumption that the phase III trials would show an improvement in overall survival.  The AVADO and RIBBON1 trials showed a benefit in progression free survival or PFS (ie a surrogate marker of event free survival), but unfortunately were not positive for overall survival, which is the ultimate measure of disease progression and the condition required to be met under the fast track process.

The FDA are therefore recommending withdrawal based on the lack of overall survival as per the accelerated agreement and Roche offering the counter argument that there was evidence of patient benefit.  That issue will no doubt continue to be debated for much of 2011 until the public hearing later this year.  There is an excellent analysis of the impact of the FDA recommendation on bevacizumab uptake in the US in Oncology Business Review for anyone interested in trends.

Ultimately, we need have a better understanding of the molecular basis of the cancer types and drugs developed to target that aberration in a more carefully selected patient population.  The arguments for and against accelerated review will run and run – probably for longer than the debate about how to pronounce some of the new names!

My position on the accelerated review process?

When it works, it works well.  However, problems can arise when you get phase III trials that do not support the full approval due to a lack of a proven overall survival advantage in the population evaluated.  The FDA can find themselves in an impossible position especially given the high emotions that run in breast cancer, for example.  The onus should be on the company to do further research or trials better defining the patients who are most likely to respond rather than risk exposing thousands of patients to the systemic effects of a drug that may not offer meaningful benefit to the majority.

References:

ResearchBlogging.orgChabner, B. (2011). Early Accelerated Approval for Highly Targeted Cancer Drugs New England Journal of Medicine, 364 (12), 1087-1089 DOI: 10.1056/NEJMp1100548

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This week heralds a busy one with the upcoming annual NY Chemotherapy Foundation (Greenspan) meeting that begins tomorrow at the Marriott Marquis in Times Square with the Pediatric session in the afternoon and finishes on Saturday with the Nursing session.

I’ll be at the Greenspan event from Weds to Fri, please do say hello if you see me around.

In the meantime, I’ve been pleasantly surprised at the number of signups to the conference newsletter (see the sign up widget in the right hand margin —>).   The first one, from AACR on colon cancer, goes out this on Wednesday week, please sign up before then if you would like to receive it.

More newsletters will follow soon on the Greenspan Meeting, ASH and SABCS.

I’ve just added a new meeting to my January conference schedule and will be attending the 6th International Society of Gastroenterological Carcinogenesis in Houston, Texas. It’s hosted by MD Anderson and you see the program here.  Many thanks to Drs Ray DuBois and Anas Younes for alerting me to the event.  There are some interesting speakers and topics so it looks like being a good meeting.

You can see my active schedule in the Conference Schedule tab at the top of the site. More events will be added for 2011 as dates firm up.

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"The systematic characterization of somatic mutations in cancer genomes is essential for understanding the disease and for developing targeted therapeutics."

So began today's journal article from a letter to Nature (link below) from scientists at Genentech.  They went on to state that they have looked at:

"The identification of 2,576 somatic mutations across 1,800 megabases of DNA representing 1,507 coding genes from 441 tumours comprising breast, lung, ovarian and prostate cancer types and subtypes. We found that mutation rates and the sets of mutated genes varied substantially across tumour types and subtypes.

Statistical analysis identified 77 significantly mutated genes including protein kinases, G-protein-coupled receptors such as GRM8, BAI3, AGTRL1 (also called APLNR) and LPHN3, and other druggable targets.

Integrated analysis of somatic mutations and copy number alterations identified another 35 significantly altered genes including GNAS, indicating an expanded role for Ga subunits in multiple cancer types."

The goal of this type of analysis is to look for patterns and alterations associated with disease and try to figure out which are potentially druggable targets for drug development.  The researchers went on to note:

"Our study represents a substantial expansion of the knowledge base of cancer somatic mutations. Of the 845 genes with proteinaltering mutations identified in this study, 361 (43%), including 13 significantly mutated genes like TLR4, SPOP and NRG3, have not previously been reported."

image from www.flickr.com That's great news. Of course, it should be noticed that theory is one thing, but until a pipeline compound enters into clinical trials and we see the results of extensive studies, we won't know whether the target is truly a relevant one in human cancers or not.

Not all mutations may occur in every person though, as we have seen in lung cancer where some people might have an EGFR mutation, some an ALK mutation and so on. The secret to this approach is to start documenting the likely targets and go looking to see how many exist, which ones might be a critical driver and which ones are merely passengers.

Clearly though, it does help to have an idea of what the needles in the haystack might look light before going hunting for them to increase the chances of success.

Photo Credit: Yellow Book

 

ResearchBlogging.orgKan, Z., Jaiswal, B., Stinson, J., Janakiraman, V., Bhatt, D., Stern, H., Yue, P., Haverty, P., Bourgon, R., Zheng, J., Moorhead, M., Chaudhuri, S., Tomsho, L., Peters, B., Pujara, K., Cordes, S., Davis, D., Carlton, V., Yuan, W., Li, L., Wang, W., Eigenbrot, C., Kaminker, J., Eberhard, D., Waring, P., Schuster, S., Modrusan, Z., Zhang, Z., Stokoe, D., de Sauvage, F., Faham, M., & Seshagiri, S. (2010). Diverse somatic mutation patterns and pathway alterations in human cancers Nature DOI: 10.1038/nature09208

A really interesting idea that seems to be growing in popularity is the concept of fluid-based biomarkers from blood, urine, saliva etc, as opposed to invasive tumour biopsies. A recent paper in Cancer Research took a look at this novel and much needed concept (reference below). 

One of the biggest challenges in oncology at the moment is finding easier and more convenient ways of identifying appropriate patients who might be best suited for a given therapy.  In clinical trials, often tests are developed as useful biomarkers based on tumour biopsies.  However, once a drug is approved, Community Oncologists often find their patients older, frailer and with a poorer performance status or more advanced disease and thus unresectable. Earlier detection of asymptomatic patients would also be useful, since in general, the earlier the patient is diagnosed, the better their long term chances are.

There is a lot of potential value, therefore, in developing fluid-based biomarkers and tests since the majority of cancer patients are treated in the Community, rather than Academic, setting.

In leukemias, FISH and QT-PCR testing have become standard, largely because it is easy to compare a blood sample with that of a bone marrow sample to validate test results.  In solid tumours though, that has generally been less easy. Even the FISH test for HER-2 positive women with breast cancer has not been without it's controversies over the years.  

At recent cancer meetings such as ASCO and AACR, I have noticed an increasing number of early surrogate markers being explored in solid tumours such as circulating tumour cells (CTCs) in prostate cancer as a more viable marker than PSA, as the authors also discussed:

"Fluid sampling has advantages over imaging as it is widely accepted, readily repeated, convenient, noninvasive, and low cost. Biomarkers in body fluids have the potential to detect a wide variety of primary tumors and metastases located throughout the body. Fluid biomarkers include a variety of components in blood, urine, or other fluids that reflect the presence of a tumor in the body. These include circulating tumor cells (CTC) and macromolecules such as lipids, proteins, RNA, microRNA, and DNA that originate from tumor cells."

Source: Martin et al.,

It was interesting to see the development of Pfizer's crizotinib in non-small cell lung cancer (NSCLC) with ALK mutations emerge recently.  While Pfizer should be applauded for the speed with which they have developed the drug after the mutation was discovered, the development of the mutation test has clearly not been without its challenges. 

A number of patient blogs complained about the time taken to produce the results from the tumour biopsies (several weeks to a month compared to say, 48 hrs for blood tests) and also in some cases, that their own physician ordered tests were not accepted, requiring another test validated by a central laboratory, sometimes with differing results. This does not augur well for an easy to use commercial diagnostic test for ALK if there are variations in the results. 

Patients with advanced lung cancer often don't have a lot of time so this will be an issue to them and their physicians. Part of the reason for the delay is that tumour biopsy tests often require DNA sequencing to be performed, which inevitably takes time. A validated blood test would have a huge advantage in terms of time and convenience, but whether it is practically possible in an example like this, I don't know. 

Whether a validated blood test is being developed in parallel isn't yet clear, but lung biopsies in the community setting are not routine in the way they are for breast cancer, for example.  Finding suitable patients will therefore be akin to looking for needles in a haystack as the data so far suggests that the number of patients who were ALK positive in the NSCLC trials that looked for the mutation was around 5%.  I'm not sure if this will extrapolate to the broader lung cancer universe though, as patients in a clinical trial are typically different from those in the general cancer population.

Meanwhile, another other interesting trend that is emerging is microRNA:

"In addition to proteins, mRNAs are promising biomarkers, and microarrays represent a powerful approach for their discovery in blood.  A study using custom spotted arrays published in 2001 identified a signature of 12 genes whose mRNA expression was elevated in peripheral blood mononuclear cells (PBMC) of breast cancer patients." 

Source: Martin et al.,

The number of articles, papers, abstracts and presentations on microRNA has increased at a tremendous rate over the last 2 years.  At the AACR Molecular Targets meeting last November, it seemed as though 1 in 3 abstracts mentioned the subject in a variety of different ways from prognosis to early resistance. This is one area I'll be following to see what interesting new concepts emerge. I've had a few requests for more information on microRNA, so this will be the topic of a forthcoming blog post.

The ultimate question as always, though, is what does this all mean?

Clearly, earlier detection of disease is useful for prognosis, but predicting the impact of therapeutic intervention is also important. If we can develop biomarkers for determining which drug might work optimally for a given patient or subset, that would alleviate a lot of the pressure on healthcare systems and reducing patient exposure to drugs that would not work. At present, there are probably more tests developed than actually used in practice, but incorporating them into large scale clinical trials as part of a battery of tests may well provide more useful information in the near future across a variety of different cancer types. 

Time will tell, but it makes a lot of sense to incorporate a vast battery of surrogate biomarker tests upfront and then track what happens over time, as the Medivation trial with MDV3100 has shown with PSA and CTC's in prostate cancer, to offer a practical example.  You never know which of the biomarkers tested will emerge as useful in any given tumour type, so testing more rather than fewer may have a higher chance of hitting the bullseye.

ResearchBlogging.org
Martin, K., Fournier, M., Reddy, G., & Pardee, A. (2010). A Need for Basic Research on Fluid-Based Early Detection Biomarkers Cancer Research, 70 (13), 5203-5206 DOI: 10.1158/0008-5472.CAN-10-0987

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As with previous meetings, I'm aggregating the ASCO tweets using three key hashtags: 

#asco10 (the official twitter hashtag) 

#asco2010 (some people are using this) 

#ascopress (for press alerts)

The stream should be live as of 3pm CST and will run for the duration of the meeting until COB on Tuesday:


Ready, Steady, Go!

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Recently, I've been observing and watching a number of interactions that I've been part of, from friends, acquaintances, clients and physicians and healthcare practitioners.  It dawned on me that no matter what we do, our satisfaction with the result of those interactions is directly tied to the involvement we go through.  

A nasty ear infection was a salutory case in point. The reaction of my old PCP practice was close to distressing so I decided to change practice, no easy decision after 10 years with the same group.  They resolutely declined to see me despite the pain and discomfort unless I paid a disputed bill even though my insurance told me it was covered and the office hadn't billed it correctly.  The staff were rude and obnoxious in the extreme.  So much for the Hippocratic Oath! 

The first time I nervously met the new Nurse Practitioner, she surprised me by being polite, thoughtful and empathetic, a world away from confrontational New Jersey style I had become used to.  In the space of 10 minutes she explained to me gently that I had a discharge and likely an ear infection that need to be seen by a specialist that day, if possible, for cleaning and treatment.

She phoned around, made an appointment for me and dispatched me 30 blocks south to see the ENT specialist.  He turned out to be equally caring, efficient and happy to take the time to explain the problem and involve me in the solution.  As a result, I felt more involved and willing to commit to the time consuming process of fixing it, which turned out to be significant in my busy schedule. Interestingly, when I in turn explained to clients what was happening, they too understood and didn't feel resentful of the necessary absences, quite the reverse with a hearty "Go get it fixed!"

That's how it should work in an ideal situation.

However, when we don't collaborate, communicate, share or participate in the process, stonewall or or worse, just promote what we want to sell without interaction, the perception of the value offered is less than optimal and the experience is unlikely to be a positive or happy one. This applies as much to the physician-patient relationship as it does to the Pharma-physician one.

In the end, the first practice I would be less than enthusiastic about recommending, while the other two I would enthusiastically recommend to others.  In fact, when we have a bad experience we often go out of our way to warn others to save them the same pain, whereas we don't always remember to pay it forward with referrals and recommendations when we have a great experience.

My own personal medical experiences recently made me think more clearly about client – vendor interactions, to good effect.  Taking the time to involve the client in the experience and take on board their ideas to make it a better product more likely makes them: 

a) more part of the process

b) more likely to be supportive and involved

c) more likely to own it

c) more likely to see the value and appreciate it.

We're all fallibly human and make mistakes, but taking the time to involve others in the process rather than pushing what we think they need is well worth the effort in the long run.  Happy clients ultimately make for more satisfied people who value what you bring to the table too.

In what ways do you think about increasing value with others around you?

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Tonight at 6pm, the ASCO abstracts of live online with the exception of the plenaries, late breakers and clinical review abstracts, which will published at the meeting.  7 policy exceptions were granted under SEC guidelines, meaning that limited information to be made publicly available in advance of the meeting:

Abstract 8010: Lenalidomide maintenance after transplantation for myeloma. 

Abstract LBA4007: The AVAGAST trial: A randomized, double-blind, placebo-controlled, multicenter phase III study of capecitabine and cisplatin plus bevacizumab or placebo as first-line therapy in patients with advanced gastric cancer. 

Abstract LBA4507: Denosumab versus zoledronic acid for treatment of bone metastases in patients with castration-resistant prostate cancer. 

Abstract LBA1: Phase III trial of bevacizumab (BEV) in the primary treatment of advanced epithelial ovarian cancer (EOC), primary peritoneal cancer (PPC), or fallopian tube cancer (FTC): A Gynecologic Oncology Group study. 

Abstract LBA4511: A randomized, double-blind, placebo controlled phase III trial comparing docetaxel, prednisone, and placebo with docetaxel, prednisone, and bevacizumab in men with metastatic castrate-resistant prostate cancer (metCRPC): Survival results of CALGB 90401. 

Abstract LBA7502: Results from ARQ 197-209: a global randomized placebo-controlled phase 2 clinical trial of erlotinib plus ARQ 197 versus erlotinib plus placebo in previously treated EGPR-inhibitor naive patients with locally advanced or metastatic non-small cell lung cancer (NSCLC). 

Abstract LBA8512: A phase III random assignment trial comparing percutaneous hepatic perfusion with melphalan (PHP-mel) to standard of care for patients with hepatic metastases from metastatic ocular or cutaneous melanoma.

Of these 7, no doubt keen investors will be interested in the first ($CELG) and last ($DCTH), and analysts will be anxious to see the denosumab data ($AMGN), but the ones that I will be most interested in are ARQ197 ($ARQL) and bevacizumab (Avastin) ($RHHYG).  We already know that the Avastin data was negative in gastric and prostate cancers, but positive in ovarian cancer from Roche's previous press announcements.  Ovarian cancer badly needs new options that improve outcomes for women suffering with the disease.

Sometimes though, the best data is not always in the plenary session, witness the Herceptin trial in adjuvant HER2+ breast cancer a few years ago when everyone stood up in a packed session and clapped because the data was simply stunning and groundbreaking. 

Tonight's peek at the available abstracts should give us some clues about what might be interesting. I'll try and schedule some quick posts this evening as I'll be out at client meetings all day tomorrow, great timing, not.

"Good Businesses" are not judged solely by better sales, profits, equity returns and sharholder value – these becoming old measures on their own.  Investors are increasingly asking  "So you made a profit – yawn – but did you also make an impact?"  This is what it takes to outperform today and tommorrow.

What about Big Pharma? Or little Pharma for that matter.

Aren't these companies founded on the ideals of delivering novel life-changing treatments to patients, transforming science into therapies, to serve patients, to deliver meaningful benefits to consumers, and to improve the quality of life?

How does this square with off-label marketing, physician payola schemes, manufacturing failures resulting in product shortages, contaminated or adulterated product, massive corporate lay-offs and outsourcing jobs elsewhere?"

via thebigredbiotechblog.typepad.com


Bruce Lehr of The Big Red Biotech Blog wrote a nice blog this morning that made me sit up and take notice.  He's right; some areas of the industry could do well to clean up their act and focus on the important things that matter rather than skimping on quality or indulging in fluff n puff marketing. And some people wonder why Pharma is held in such distain akin to oil or tobacco companies?

Meanwhile, in the oncology arena, we're always running head to head trials, figuring out how to beat the standard of care and improve overall survival. In other words, finding the compounds that give an edge and make an impact.

It's easy to forget that many other areas of the Pharma business live in fear of not winning, not making blockbuster revenues and thus run an inordinate number of placebo controlled rather than head to head trials. After wading through a mass of non-oncology data at the weekend, I was left wondering, "How on earth do you prove your product is better in that situation?"

If you can't beat the competition, why bother?

Which takes us back to the original review article from Umair Hague in the HBR on why Betterness is Good Business and how great companies focus on the stuff that matters, rather than just profitability and increased shareholder value.

So, I think I'll stick with the dog eat dog mentality in oncology, where we focus more on people and trying to make a difference to the lives of people with cancer. If your compound doesn't beat the standard of care it effectively dies in that indication. My firm belief is if you focus on bettering the competition, the rest will follow naturally and organically. That doesn't mean that some don't fall off the wagon and transgress into the dreaded off-label promotion though.

Still, maybe the rest of Pharma could learn a thing or two from oncology?

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