oncology | Pharma Strategy Blog

What's hot in oncology? A review of 2009 and predictions for 2010

By MaverickNY on December 18, 2009

Back in February, I took a big picture look at some of the cancer drugs in development that might be reviewed by the FDA for approval in 2009.

You can see the review here.

Of the eight drugs that were highlighted in the post, all were discussed by ODAC, so that was a positive sign. Five (Afinitor in RCC, Folotyn and Istodax in t-cell lymphomas, pazopanib in RCC and Arzerra in CLL) all passed the final hurdle, receiving a positive FDA opinion, while others (clofarabine, trabectedin and denosumab) were less lucky and issues associated with the filings are still being discussed. The EU CHMP has issued a positive opinion for Prolia (denosumab) but the FDA seem less convinced so far and issued a complete response letter requesting further information before giving approval. Amgen seem confident of addressing these issues, so we may well seen a green light soon.

While Genzyme and Amgen should be able to resolve the concerns successfully and will likely obtain FDA approval in 2010, J&J may well be left at the altar again with Yondelis. The drug was approved in Europe for soft tissue sarcomas, but approval in ovarian cancer is being sought in the US and ODAC had major issues with the trials and the risk-benefit trade-off. Time will tell what will happen in 2010.

AstraZeneca have not had a lot of luck with their pipeline since the infamous Iressa troubles. This year, they withdrew their filing for Zactima, a combination VEGF/EGFR inhibitor with limited efficacy over existing therapies. It will be interesting to see if they rebound in 2010.

The most promising robust oncology pipelines at the moment are probably those of Roche/Genentech, Novartis and Pfizer. Merck, BMS and GSK also have some interesting solid bets in their pipelines, but are not renowned for their speed of R&D and marketing in oncology compared to the other three, who are much more aggressive and focused in their resources and efforts.

W2W4 (what to watch for) in 2010?

That's the big question I'm getting in my email bag this month.

2010 is going to be an interesting year for CML patients, who will see a lot of new activity. ChemGenex filed omacetaxine for T315i mutations and treatment in patients who had failed existing TKI therapy. They have an ODAC in February and based on the data presented at ASH this month, I think they have a good chance of approval.

Novartis and BMS are both expected to submit an NDA to both the FDA and EMEA for approval of nilotinib and dasatinib respectively, in newly diagnosed CML. The nilotinib data was presented at ASH and clearly showed a 12 month efficacy benefit over imatinib, the current standard of care. We are still awaiting the dasatinib vs. imatinib data, hopefully it will be presented at either ASCO or EHA. My guess is that we may well see approvals for both drugs in the front-line setting in 2010.

The biggest challenge both companies may well have though, is not getting approval per se from the EMEA, but rather getting past NICE in the UK given the disparity in price with imatinib, when 60-70% of patients do well on the drug and attain a complete cytogenetic response at 18 months. Currently, NICE has declined to approve the second generation TKI's even in the relapse/refractory/resistance setting, so that does not augur well for the frontline setting.

Genzyme will likely have data from randomised trials with clofarabine in elderly AML in 2010, which means that approval may well be possible if the data is positive.

Cell Therapeutics presented data at ASH on pixantrone in 3rd line NHL, with evidence of activity. This drug will be another candidate for approval and the ODAC is currently scheduled for April, according to the company.

Ariad, a biotech based in Boston, have two promising agents in development. Ridaforolimus is an mTOR being developed in soft tissue sarcomas with Merck in the second line setting. I think this agent is promising, but the placebo controlled trial design in a heterogeneous disease where some subsets respond well to therapy and some are insensitive makes me nervous what the final phase III results will bring. In such an allcomers trial, you run the risk that the responders will be drowned out by the non-responders. Of course, screening out subsets in a fairly uncommon disease makes for slower accrual and time to market so the risk is a high one. What I do know is that KOL's I spoke to who participated in the trial noted that those patients who did respond tended to do very well in a heavily pretreated setting. We should know by ASCO whether Ariad's big play paid off or not.

Ariad also have a interesting agent in development for CMl, which targets the T315i mutation, currently a gap not met by the current TKI's approved on the market. Given my interest in CML, this is a new agent worth following. The early phase I data presented by Dr Cortes from MD Anderson at ASH this month looked very encouraging indeed.

Dendreon's Provenge is always a controversial topic on this blog. I'm not going to make any predictions about the vaccine this time other than to say it will be fascinating to see what happens next year! It's been somewhat of a roller coaster ride so far and I suspect that trend will continue in 2010.

J&J and Cougar's abiraterone may have enough data in prostate cancer by ASCO mid year to determine if they have enough evidence for a filing too. If so, it could be an interesting year in prostate cancer given very little new therapies have made any headway in the middle to advanced settings in extending hormone sensitivity and delaying time to progression to metastases. If either of these drugs can achieve that lofty goal, it will be very good news indeed.

Medivation also have a novel compound (MDV-3100) in much earlier development, so while the others test the regulatory waters, we can see how the new partnership evolves with Astellas.

Two other compounds I'm watching are Novartis' Antisoma compound, ASA404, in lung cancer and ipilimumab in melanoma and prostate cancer from BMS. Both of these agents have shown early signs of efficacy, so data at ASCO may well tell us whether they look like showing real promise or turning into duds.

This year saw the evolution into the limelight from the PARP inhibitors, most noticeably sanofi-aventis and BiPar's BSI-201 in triple negative breast cancer and AstraZeneca and KuDos's AZD2281 in BRCA1 and 2 mutated cancers such as breast and ovarian. I'm really looking forward to seeing the latest data at ASCO in June 2010 after following their progress at ASCO and AACR this year.

So of all the new pipeline drugs mentioned in this post, what is particularly compelling? I'm probably most excited by the PARP inhibitors and ASA-404, all of which have a real chance to stand out from the crowd. We'll see this time next year whether that turns out to be a good prediction or not!

Further updates of interesting compounds in development will continue o
n this blog next year.

Of course, if anyone has any other favourites they're following in oncology, please add them in the comments or drop me an email. We'd love to hear what others think.

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Between the Lines – Proto Magazine – Massachusetts General Hospital

By MaverickNY on December 2, 2009

By using language- and pattern-analyzing software to search and distill the cascade of words on social networking sites, researchers may be able to identify trends and signals, such as repeated mentions of a certain drug in connection with a particular side effect or treatment success. “Listening” to thousands of patients as they discuss treatments, side effects and experiences with their diseases might even help scientists come up with hypotheses worthy of study. “There’s a tremendous amount that goes on in a patient’s daily life,” says Frank Moss, director of the Massachusetts Institute of Technology Media Lab, an emerging-technologies research group that helped create one disease-related networking site, and a founder of the cancer drug company Infinity Pharmaceuticals. “They’re trying off-label drugs, different diets, different exercise, different lifestyles. That information isn’t easily available to clinicians, but the cure to the disease may lie within it.”

via protomag.com

This is an excerpt from the Massachusetts General Hospital quarterly magazine, Protomag, which you can also read online, via the link above.

The article isn't just about data mining, but also about how patients can connect and converse about their disease through forums as well as the dangers of social media sites that are unchecked by authorities (viz the FDA).

The 'deep web' as Gilles Frydman described it in the comments to the recent post on this blog about the FDA, social media and patients, has both advantages and disadvantages. One the one hand, it is a great resource for people needing advice from others with the same condition and on the other, it can be a fertile ground for misinformation and unscientific data with no substance or rigour.

Check out the full article in Protomag, it's well worth reading.

Posted via web from sally church's posterous

ASH – what's hot news this year?

By MaverickNY on December 2, 2009

On Friday, many of us interested in hematology and oncology will be heading to New Orleans and the annual American Society of Hematology (ASH) meeting. Every year, I like to try and predict what might be hot topics beforehand, although I'm not always right!

So without breaking any embargoes, based on companies, drugs, and data that I've been following this year, here's my list of Pharma companies to watch out for:

Celgene: Revlimid is doing well in the refractory setting and will likely have some stunning data in the front-line setting in multiple myeloma. Data was released in July this year suggesting that patients live longer on the drug, paving the way for maintenance therapy as a viable option. This is not good news for Millennium and J&J in the long run, who promote Velcade. However, in the short term, Millennium still have a huge advantage over their rivals given they they have demonstrated long term survival data in the newly diagnosed setting, which Revlimid does not have. It's clearly time to step up the R&D and marketing efforts a few notches now that the competition is getting hot. Millennium do have a promising neddylation inhibitor, MLN4924, up their sleeve and I'm looking forward to seeing the latest data on that too.
Novartis: Tasigna front-line data is being presented as a late breaking abstract suggesting that is achieves deeper and earlier complete cytogenetic responses than Gleevec, the standard of care. It looks like the company will have likely beaten BMS and Sprycel in the race to file the 2nd generation TKI's in newly diagnosed CML. Afinitor is being developed beyond renal cell carcinoma in many indications, including NHL.
GSK: Arzerra has now been approved for the treatment of chronic lymphocytic leukemia (CLL) in patients who have become refractory to fludarabine and alemtuzumab. Updated data in NHL is expected at this meeting.

Biotech companies also look to be well represented, although most of the data will be phase I and II, rather than big phase III studies:

Onyx/Proteolix: Carfilzomib is a 2nd generation proteasome inhibitor that appears to spare patients some of the peripheral neuropathy associated with Velcade. The agent has been doing well in trials to date and new, mature data is expected at ASH.
Ariad: AP24534 is a TKI which appears to inhibit the T315i mutation not targeted by imatinib, dasatinib or nilotinib. Although this mutation is rare, it is fatal as there are no approved options to target it at present.
AEtena Zentaris/Keryx: Developing perifosine in myeloma. Combination data with Velcade and dexamethasone is expected to be presented at ASH, see the link to the press release on the poster below.
Seattle Genetics: Have had a rocky ride lately with the halting of dacetuzumab in combination with rituximab in diffuse large cell B-lymphomas but are presenting an update at the meeting. They have another compound, brentuximab, in development for CD-30+ lymphomas.
Trubion: TRU-016 is an anti-CD37 small modular immunopharmaceutical (SMIP™) protein in development for CLL, which they licensed from Facet. It's far to early to tell whether this agent has any promise, but worth watching, just in case.

Of course, there are also some others, such as Allos Therapeutics pralatrexate and Gloucester Pharma's romidepsin, but these have been recently approved in rare forms of NHL, ie PTCL and CTCL respectively. It will be interesting to see how and where they plan to expand to other indications outside the orphan drug designated initial approvals.

Calistoga and Semafore are both developing PI3 Kinase inhibitors in hematologic indications such as refractory B-cell malignancies and myeloma, respectively. The data is still very immature, being phase I trials, but worth looking at since many of the big pharma company PI3 kinases are being tested in solid tumours rather than hematological cancers.

I'll be posting daily reports from the ASH meeting, so watch this space!

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Adjuvant Hormonal Therapy for Breast Cancer and Risk of Contralateral Breast Cancer

By MaverickNY on August 26, 2009

Compared with the breast cancer risk women in the general populationhave, breast cancer survivors have a substantially higher riskof developing a second primary contralateral breast cancer.Adjuvant hormonal therapy reduces this risk, but preliminarydata indicate that it may also increase risk of hormone receptor–negativecontralateral tumors. We conducted a population-based nestedcase-control study including 367 women diagnosed with both firstprimary estrogen receptor (ER)–positive invasive breastcancer and second primary contralateral breast cancer and 728matched control women diagnosed only with a first breast cancer.Data on adjuvant hormonal therapy, other treatments, and breastcancer risk factors were ascertained through telephone interviewsand medical record abstractions. Two-sided statistical testsusing conditional logistic regression were conducted to quantifyassociations between adjuvant hormonal therapy and risk of hormonereceptor–specific subtypes of contralateral breast cancer(n = 303 ER+ and n = 52 ER- cases). Compared with women nottreated with hormonal therapy, users of adjuvant tamoxifen for5 years had a reduced risk of ER+ contralateral breast cancer[odds ratio, 0.4; 95% confidence interval (CI), 0.3–0.7],but a 4.4-fold (95% CI, 1.03–19.0) increased risk of ER-contralateral breast cancer. Tamoxifen use for <5 years wasnot associated with ER- contralateral breast cancer risk. Althoughadjuvant hormonal therapy has clear benefits, risk of the relativelyuncommon outcome of ER- contralateral breast cancer may nowneed to be tallied among its risks. This is of clinical concerngiven the poorer prognosis of ER- compared with ER+ tumors.[Cancer Res 2009;69(17):6865–70]

via cancerres.aacrjournals.org

Hormonal therapy with drugs like tamoxifen is one of the most common treatments for breast cancer because it has been shown to reduce the risk of dying from the disease but, as this study now suggests, there are long term risks associated with the treatment.

Thus we see that on one hand, long-term tamoxifen use among breast cancer survivors decreases the risk of developing the most common, less aggressive type of second breast cancer, but on the other, such use is associated with a more than four-fold increased risk of a more aggressive, difficult-to-treat type of cancer known as ER-negative disease in the breast opposite to the initial tumor.

At this stage, it isn't clear what the mechanism for the development of ER-negative contralateral disease is, but it is worrying risk given the poor prognosis associated with the disease.

Posted via web from sally church's posterous

Li, C., Daling, J., Porter, P., Tang, M., & Malone, K. (2009). Adjuvant Hormonal Therapy for Breast Cancer and Risk of Hormone Receptor-Specific Subtypes of Contralateral Breast Cancer Cancer Research, 69 (17), 6865-6870 DOI: 10.1158/0008-5472.CAN-09-1355

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Clinical trial results show Denosumab is superior to Zometa in breast cancer patients with bone metastases

By MaverickNY on July 13, 2009

Amgen’s recent announcement of phase III trial data showing that it’s monoclonal antibody, denosumab was superior to Novartis’ Zometa (zoledronic acid) for the treatment of breast cancer patients with bone mestastases is further news that scientifically driven drug development can yield exciting results.

Denosumab is in essence a targeted therapy like Gleevec, Avastin or Herceptin. It’s development came about from basic research that discovered the cellular control of bone remodelling and regulation of bone density is reglated by the RANK Ligand pathway.

RANK Ligand is a TNF famly member, a protein that is expressed on the sufrace of marrow, stromal cells and osteoblasts (the cells responsible for bone formation). When RANK-L binds with its receptor RANK it stimulates the activity of osteoclasts (cells responsible for bone resorption). In the body, RANK-L production is naturally regulated by the protein Osteoprotegerin (OPG), which binds with RANK-L thereby preventing it from binding to its receptor, RANK. When there is insufficient OPG, or too much RANK-L produced, excess bone loss occurs. This occurs in post-menopausal women or in cancer related bone loss.

Denosumab acts by attaching itself to RANK-L, thereby inhibiting its action. Deprived of RANK-L, osteoclasts cannot form, function or survive. The result is less bone destruction and bone loss. Understanding the RANK Ligand pathway has been a breakthrough step in understanding bone biology.

Many cancer patients end up with bone metastases that not only causes pain, but also bone destruction. Roodman, in a 2004 New England Journal article, proposed the “vicious cycle” hypothesis to explain this: Tumor cells produce parathyroid hormone-related peptide (PTHrP), which stimulates osteoblasts to produce RANK ligand leading to less production (downregulation) of osteoprotegerin (OPG), thereby stimulating osteoclasts to resorb more bone. At the same time, production of PTHrP promotes tumor growth directly. Therefore, it should come as no surprise that denosumab would be effective in cancer patients with bone mets and skeletal related events.

What does the future hold for denosumab? In the postmenopausal osteoporosis market, a once or twice yearly injection is extremely attractive given its ease of use. Compliance is a real issue with bisphosphates such as alendronate or risedronate where a daily pill must be taken. Many primary care physicians are not set-up to administer an infusion, which is what Novartis’ once a year osteoporosis treatment, Reclast requires.

However, despite impressive clinical data, Amgen does not yet have a home run. It lacks a large sales force and infrastructure to sell to primary care physicians. Also with generic fosamax (alendronate) available, the cost/benefit trade off is going to be a key factor in uptake. The cost of denosumab will need to be carefully considered for Amgen to enter this competitive market. The FDA advisory board meets on August 13 to discuss Amgen’s BLA application and consider whether to recommend approval for the treatment and prevention of osteoporosis, and treatment of bone loss in patients undergoing hormone ablation for prostrate and breast cancer. Given the positive data from the phase III pivotal studies, a positive recommendation is expected with approval by the FDA expected in October.

For cancer patients, denosumab could become the gold-standard for treatment of bone metastases given its superiority over Novartis’ Zometa. For oncologists, the fact that denosumab only requires an injection while Zometa requires an infusion is less of an issue. The key to success for oncology drugs is based solely on the data. If the positive results continue, Amgen are likely to take market share from Zometa once approval for the treatment of bone metastases is obtained in 2010 or 2011.

So, my take on this is that denosumab is a real winner for Amgen. Whether it will capture the market for postmenopausal osteoporosis remains to be seen, but it is an exciting new drug that will benefit cancer patients. Further data on denosumab can be expected from the September meeting of the American Society of Bone and Mineral Research (ASBMR) in Denver.

Market driven strategies are very simple at heart

By MaverickNY on June 9, 2009

The other day I was mapping out a basic marketing plan for a pharma client and realised that I was in grave danger of thinking too much. Why? Because while there are many many components of a marketing plan, indeed, any strategic plan, sometimes simple is better.

Here's the complex plan I started, and thankfully, never finished. It looked something like a dark ominous spiders web (a function of the NY weather this morning when I took these shots for the blog):

The actual detail doesn't matter, you get the gist that things can get quite complicated even when you look at the big picture. Now, while drawing more various components on another sheet, I realised this morning that things could be simplified in a way that would focus the goals on the real objective, which is how can the product compete when it's 24th (or whatever) to market. You see, marketing and a market driven strategy at it's heart is very straightforward. It's just we humans who sometimes over complicate things. Instead, it is often better to think about what is the very essence things can be distilled down to?

Take a look a this – simpler, cleaner and altogether more obvious:

What this more elegant approach allowed me to do was stimulate discussion on the teleconference around the key issues, namely what is happening in the market now, what do we know about what the unmet medical needs are and what could the new product in development possibly do differently, if positioned towards those unmet medical needs.

With the original, I just took a photo on my iPhone and emailed it over. Then, the brainstorm was captured on a whiteboard during the teleconference, photographed on a Blackberry and emailed back to me. Who needs to waste time drawing fancy slides when you can have instant communication remotely?

We're now all clearer which needles in a haystack we can test for in market research rather than wasting time looking for needles in a haystack and vaguely hoping the physicians will tell us. We can use web2.0 tools and social media monitoring to mine for what consumers think, but at least we will know what we're looking for. After all, you wouldn't expect a blindfolded archer to hit a target he can't even see.

Ultimately, it's not about being first to market but about thinking and listening so that the product you create is simple and meets redefined needs. Sometimes, simple ideas from thinking outside of the box can give you new glimpses about what might be possible if you reframe the questions to start with.

That's the true value of insights and thinking clearly rather than getting bogged down in analysis by paralyis.

What we are ultimately trying to achieve with new medical treatments is find a way to match a therapy with a particular group of patients, but very few Pharma marketers actually remember this:

Apologies for the dark cartoons, they are hardly Hugh's standard 🙂

Thoughts and ideas from folks? What approaches have you found useful?

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After the Inauguration, time to get back to work

By MaverickNY on January 21, 2009

President Obama's speech yesterday at the Inauguration yesterday was a good one for me. When was the last time you heard an incoming President actually mention science, health and technology? I posted the full text of the speech on my Tumblog, but here is the except that excited and surprised me:

"We will restore science to its rightful place, and wield technology’s
wonders to raise health care’s quality and lower its cost. We will
harness the sun and the winds and the soil to fuel our cars and run our
factories. And we will transform our schools and colleges and
universities to meet the demands of a new age. All this we can do. And
all this we will do."

Now, I'm not sure what science's rightful place is, but at least a President who is not afraid of it and is willing to debate the merits is an excellent start. With regards to technology in health care, my sense is that it tends to increase costs not lower it, although I'm willing to have an open mind on that. There was an interesting article in this morning's WSJ Health blog about encouraging e-prescribing amongst physicians for Medicare drugs:

"Medicare this month began paying doctors a bonus if they switch their
patients over to e-prescribing. Some private health plans also have
begun offering extra payments along with free equipment, such as
digital handheld devices. And a coalition of technology companies is
giving doctors free software to encourage them to ditch their paper
prescription pads. As a result, the number of physicians prescribing
medicines electronically has more than doubled in the past year to
about 70,000, or about 12% of all office-based doctors."

This is all very interesting and I'm sure it reduces the number of prescribing errors from mis-read or poorly written prescriptions, but whether costs are saved (other than trees) is another matter entirely.

Science and technology can definitely improve healthcare in the form of improved quality of life or longer survival times for cancer patients, for example. This is usually accompanied by an increase in price and overall costs, just as many other goods and services increase over time. With the oil crisis forever in people's mnds, science and technology can probably most impact the environment and future energy sources. Scientific American posted an interesting article on that very topic recently.

Either way, we begin with a bright new day, a new President and hope for the future. I can't help wondering what a better situation we might have been had Reagan had the foresoght and imagination to spend serious dollars on science and technology for health or energy resources instead of missiles and the Star Wars space screens 20 years ago. Each new Administration may do their work in the present, but their actions (and lack of them) affect future generations significantly.

They will ultimately be judged and remembered by their lasting legacy.

New simple strategies for enhancing cancer chemotherapy treatment

By MaverickNY on January 12, 2009

Patients undergoing treatment for cancer with chemotherapy may often not receive the optimal drug combination or dosing for a number of reasons. These include debilitating side effects, high interstitial fluid pressure, leaky vessels or the development of tumour resistance.

In recent years, researchers have started to look at novel ways of making treatment more effective. On such way is to change the formulation, develop more targeted agents that specifically inhibit the abnormal protein or better sequencing of available therapies. Some of these have had mixed success as the stories of Gleevec, Tarceva, Iressa and Avastin have shown, albeit in some, but not all patients.

Image via WikipediaLung cancer, or more specifically, non-small cell lung cancer (NSCLC), which affects 80% of lung cases, has a very low response to chemotherapy with only 20% typically experiencing tumour shrinkage and an survival rate on average of 10-16%. New approaches are desperately needed in this disease as well as basic research underpining greater tumour specificity. At present, standard chemotherapies used in NSCLC target not only the lung cancer cells but also normal cells, thereby increasing the burden of drug toxicity and reducing the chances of overall success.

An interesting idea that has just been investigated by Taiwanese researchers in NSCLC is the use of a novel peptide to overcome the therapeutic effectiveness of drug delivery:

"We isolated a novel peptide ligand from a phage-displayed peptide
library that bound to non-small cell lung cancer (NSCLC) cell lines.
The targeting phage bound to several NSCLC cell lines but not to normal
cells."

This interesting and specific approach was tested in mice and led to a 5-7 fold increase in the drug accumulation inside the carcinoma. This should lead to greater chance of apoptosis (cell death) of the cancer cells and thus improved tumour shrinkage. The authors concluded that:

"The current study suggests that this tumor-specific peptide may be used
to create chemotherapies specifically targeting tumor cells in the
treatment of NSCLC and to design targeted gene transfer vectors or it
may be used one in the diagnosis of this malignancy."

Although the idea is an early one, we may soon see the approach used with existing chemotherapies inclinical trials in the near future. While there is no guarantee that the mice results will translate to humans, it is certainly an idea worth trying.

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Genetically modified purple tomatoes, anti-oxidants and cancer

By MaverickNY on October 28, 2008

Tomatoes genetically modified
to be rich in antioxidants called anthocyanins appeared to extend the life
spans of cancer-prone mice, according to a study reported via letter in Nature Biotechnology.

The modified tomatoes were created by adding two genes (Delila and
Rosea1) from the snapdragon flower. The anthocyanins, which belong to the
flavonoid class of antioxidants, gave the tomatoes a peculiar purple
colour.

The two genes that were isolated are responsible for flower pigmentation
and, when introduced in other plants, turned out to be the perfect
combination to produce anthocyanins, the same phytochemical found in
blueberries. Anthocyanin is thought to have anti-cancer properties.

Chemical tests revealed that the purple tomato has a very high
antioxidant activity, almost tripled in comparison to the natural fruit,
making it very useful to study the effect of anthocyanins.

The researchers fed a powder obtained from the purple tomatoes to mice
that lacked the p53 gene, which helps protect against cancer. These mice
had an average life span of 182 days compared to 142 days for
p53-deficient mice fed a standard diet.

The significance of these findings?

According to one of the researchers quoted by the BBC:

"Most people do not eat five portions of fruits and vegetables a day,
but they can get more benefit from those they do eat if common fruit
and veg can be developed that are higher in bioactive compounds."

Overcoming resistance to treatment with EGFR inhibitors

By MaverickNY on October 28, 2008

In a preclinical study presented at the EORTC-NCI-AACR meeting, a compound known as XL184 (Exelixis), showed
encouraging results in boosting sensitivity to erlotinib (Tarceva) and gefitinib
(Iressa) in drug-resistant lung cancer.

Gefitinib and erlotinib belong to a
class of targeted drugs that target the epidermal growth factor
receptor (EGFR) gene, which is mutated in many non-small cell lung
cancers (NSCLC).

MET kinase, which is inhibited by XL184, is implicated in the
resistance to EGFR kinase inhibitors. This approach potentially has the opportunity to turn the resistance mechanisms off, thereby allowing Tarceva to work more effectively in NSCLC when taken in combination with a MET kinase inhibitor such as XL184.

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Posts tagged ‘oncology’