Clovis Oncology – A buying opportunity following the EOS deal

Last week, Clovis Oncology (CLVS) announced the acquisition of EOS, a small Italian company with an oncology program in phase II. To me, this is the smartest deal in 2013 so far given the relatively low price ($200M) Clovis paid for a mid stage oncology asset with a strong clinical proof of concept and a clear differentiation from competition. Clovis has commercialization rights for US and Japan while Servier has EU+ROW according to a previous licensing agreement with EOS.

EOS’ drug, lucitanib (E-3810) is a dual VEGF/FGF pathway inhibitor. The FGF pathway became a popular target based on the high incidence of FGF pathway activating mutations in many tumor types. In addition, the FGF family is implicated in general cancerous processes such as angiogenesis and migration. While the VEGF pathway has been successfully pursued with small molecules (Sutent, Inlyta, Nexavar), unlocking the therapeutic potential of the FGF pathway proved more challenging.

One of the reasons for the limited success lies in the complexity of the FGF network which includes 4 receptors and over 20 different ligands with diverse biological functions. Another reason may be the fact that even in patients whose tumors have FGF pathway activation, inhibiting the pathway alone is not sufficient for a pronounced clinical effect. In other words, “FGF-positive” cells are not addicted to FGFR signaling the way cells with other mutations (ALK, EGFR, BRAF) are addicted to their respective mutations.

Lucitanib has the right selectivity profile

There are many (>10) small molecule FGFR inhibitors in development.  Some (Novartis, Ariad, Boehringer Ingelheim) developed  broad spectrum drugs that inhibit multiple targets on top of FGFR (in some cases FGFR was not the primary target) whereas others (Astra Zeneca, Novartis, Lilly) developed more selective FGFR inhibitors. Although, both approaches have their merits, the general trend today favors selective inhibitors (especially in biomarker defined populations) due to their ability to maximally hit the desired target without unnecessary toxicity.

Lucitanib falls somewhere in the middle. It is not a pure FGFR inhibitor but it inhibits only a handful of additional targets (predominantly VEGFR).Within the FGFR and VEGFR families, lucitanib inhibits FGFR1 and VEGFR2 (both considered the primary receptors in their respective network) with similar potency. This appears to be a distinguishing property that may explain why lucitanib is the only FGFR inhibitor with good clinical activity.

Another unique feature of lucitanib is strong inhibition of CSF1R, which was noted in EOS’ presentations but not in Clovis’ recent presentation. Nevertheless, it is not clear whether CSF1R is involved in the drug’s activity.

Clinical results       

Lucitanib’s clinical proof of concept comes from a small cohort of breast cancer patients whose tumors had activation of the FGF pathway (FDF+).Of 12 evaluable patients 6 (50%) achieved a partial response (5 confirmed) and 5 achieved disease stabilization with a median progression-free survival (PFS) of 9.4 months. Despite the small sample size, this response profile cannot be coincidental and compares very favorably with other FGFR inhibitors which have demonstrated little to no effect in similar patients. As a benchmark, Kadcyla, which is considered a breakthrough drug in HER2+ breast cancer, had a response rate of 38.4% and a PFS of ~5 months in phase II.

The most provocative finding was the impressive activity lucitanib had in some patients who had previously failed other FGFR inhibitors. Clovis’ presentation reports 4 such patients, all of whom were on lucitanib much longer than on prior FGFR inhibitors. One patient, who progressed on Novartis’ (NVS) selective FGFR inhibitor after 2 weeks, is still on lucitanib for 21 months. This provides the ultimate proof that lucitanib is a best-in-class FGFR inhibitor.

lucitanib

Commercial opportunity

Lucitanib’s addressable market is significant based on the high incidence of FGF+ tumors across multiple tumor types. The opportunity in breast cancer alone (23.7% of cases) is comparable to the HER2+ segment, which represents a $1B market in advanced stage disease (excluding adjuvant therapy). FGF activation has been documented in other tumors including lung, ovarian and head and neck cancer. FGFR1-amplified lung cancer appears particularly promising, as there are efficacy signs in this indication with other FGFR inhibitors. FGFR1 amplification occurs predominantly in squamous-NSCLC, which are not candidates for Avastin due to safety concerns. The risk-reward profile of a dual VEGFR/FGFR inhibitor in these patients is yet to be evaluated.

Competition

There are over 10 active programs for FGFR inhibitors as well as multiple antibodies in development. To date, lucitanib remains the only drug with compelling activity (others have shown limited to no activity in FGF+ tumors) and it may be the only drug to be approved as monotherapy.

Results to date imply that selective FGFR inhibitors are not sufficiently active in humans and that VEGFR inhibition is required to potentiate the effect. There are only 2 other drugs with a similar selectivity spectrum (selective FGFR1/VEGFR2): Lilly’s (LLY) LY2874455 and a compound developed by Advenchen, which discovered lucitanib before licensing it to EOS.

Selective FGFR inhibitors such as Novartis’ BGJ398 and AstraZeneca’s (AZN) AZD4547 must be combined with VEGFR inhibitors in order to replicate lucitanib’s activity in FGF+ patients. Although technically this can be achieved even through co-formulation in the same capsule, finding the exact regimen and dose ratio is not always straightforward. On the other hand, using 2 distinct drugs allows for flexibility in dosing regimen and ratios.

Most of the VEGFR inhibitors (approved or in development) are not selective and combinations may be too toxic. The only truly selective VEGFR inhibitor is Aveo’s (AVEO) tivozanib. Its selectivity and ideal safety profile make tivozanib an ideal candidate for combination with selective FGFR. Novartis and AstraZeneca are pursuing combinations with several drugs but not with VEGFR inhibitors.

Portfolio update

We are initiating a position in Clovis, which now has 3 potential blockbusters with clinical proof of concept and biomarker-defined target populations. We are also selling Gilead (GILD) for a profit of 250%.

Portfolio holdings – December 1st 2013

Biotech portfolio - Dec 1st 2013- after changes

biotech etfs - Dec 1st 2013

90 thoughts on “Clovis Oncology – A buying opportunity following the EOS deal

  1. Alex65 – It’s always better to see insiders buying but the fact he sold share simplies there is no imminent catastrophy. The most important near term event is this weekend at ASH, where they need to show better response rate in CLL or at least a couple of responses in ibrutinib failures.

    Re tivo, I wouldn’t buy AVEO just because I think it will be a perfect match for selective FGFR inhibitors. Nevertheless, if I were AZN or NVS, I would try to combine my selective FGFR inhibitor with tivo and hope to get a better clinical profile.

    Ohad

  2. Thanks for the info as it pertains to AVEO. I was already long AVEO for the multiple shots on goal still remaining for tivozanib (starting w/CRC biomarker data in 2014), ficlatuzumab, AV-203, cachexia antibody in pre-clinic, and given fact shares trade below cash now. Didn’t realize that at least the potential is there that others could have interest in tivo to pair it with their respective FGFR inhibitor.

  3. P.S. Ohad, on CLVS, just curious as to what you see as upside potential for CLVS shares here. Shares have already had a nice run and the company sports close to a $2B market cap now. Just curious on upside potential from this valuation. Thanks.

  4. That was my initial concer too, i.e how much higher can a company with 3 drugs be worth.
    I haven’t done a serious model of sales projections but I think there is a high likelihood for both lucitanib and CO-1686 to receive accelerated approval in 2015-2016. When you look at relevant benchmarks, the 2 drugs can generate sales of $1.5B combined using fairly conservative assumptions in treatment refractory patients. Using a 5-7 sales multiple and discount it should support 3-4X increase with 18-24 months.

    Ohad

  5. Thanks Ohad. From the opposite standpoint, do you know any big pharma (or others) that have VEGFR inhibitor but may be lacking FGFR inhibitor? Just curious in sense of if any key players out there that could have interest in ARQL FGFR inhibitor (don’t think it also hits VEGFR) to combine with their own VEGFR.

  6. There are a lot of VEGFR inhibitors out there (basically every pharma has one) but most are not VEGFR selective which might make them unsuitable for combinations. I also played wit the idea of combining AVEO’s tivozanib with ARQL’s ARQ087 but turns out ARQ087 is not very selective (although it doesn’t hit VEGFR2).

    Ohad

  7. Ohad, Agree, great deal by CLVS, especially by using its relatively expensive stock as currency. As of similar compounds in clinical development, I’d say the one with most clinical data is BMY’s Brivanib – never seen any data in FGF+ cancers though.

  8. Ohad,

    Do you have an opinion on BIND? It’s come down quite a bit from its IPO price.

  9. Ohad, can you clarify what you mean with your comments on ARQL’s ARQ087 FGFR inhibitor not being very selective? I’m not aware that it hits anything beyond FGFR (curious to hear if you know otherwise) and while I think it primarily hits FGFR2, I think there is activity against FGFR1 as well. But, again, not sure what else it hits beyond FGFR in general, if anything.

  10. Davidmmp – From what I understand, the ASTX/JNJ compound is FGFR selective with limited VEGFR2 activity. They even presented how they elimiated initial VEGFR2 inhibition. Do you have info implying otherwise?

    JQ – I wouldn’t view brivanib as a serious competitor, it is more selective towards VEGFR2.

    Richard – As I wrote in the past, the concept and preclinical data are exciting but the clinical data is underwhelming (to date).

    mcbio – Based on the posters I have ARQ087 inhibits many targets in the nanomolar range including RET, DDR, FMS and PDGFR. I believe the posters are available on ARQL’s web site, if you want shoot me an email and I can send you the relevant one.

    Ohad

  11. Hey Ohad
    Yes, CLVS. I like the company too. I was just worried about their valuation at this point. So thanks for you words on where you think it may go. You mention possibly three blockbusters for the company (I know the EOS drug, CO-1686), which would be the third?

    Have you looked at the newly announced pivotal study (Metric) for CDX-011, also, what do you think of their CDX-014 drug, which targts TIM-1. It was mentioned as the next drug to go to phase one. CLDX management thinks it will be used in combination with many other immuno-boosting drugs.

    Thanks once again for your advice

    Dan

  12. One more question…
    how does a drug like Lucitanib compare to MGCD265 / they are both targeting multiple pathways, with the VEGRF1-3 overlap. There may also be overlap with teh sonditions they treat. At this point MRTX valuation is $160M. Lower than the value CLVS paid for Lucitanib. However there is less data available on MGCD265.
    Thanks
    D

  13. Alex – Sorry, can’t comment on Israeli companies.

    Dan – the third program is lucaparib (PARP). Re CLDX , don’t have anything smart to say anout METRIC, looks in line with what they promised.
    CDX-014 is one of the Curagen programs, I wasn’t aware of the fact they plan on developing it. Mentioning it in the context of immune modulation is strange, unless they plan on using a naked antibody. As an ADC, TIM1 is just an overexpressed target. Any way, I am glad to hear it is being advanced.
    As a target, TIM3 is receiving a lot of attention as an immune checkpoint, TIM1 to a lesser extent.

    Ohad

    Ohad

  14. Dan – I don’t think lucitanibn and MGCD265 compete despite the VEGFR overlap. Importantly, lucitanib demonstrated great activity in biomarker defined patients, MGCD265 didn’t (yet). If I had to choose between CLVS and MRTX at the current valuations, CLVS it is!

    Ohad

  15. Great article Ohad. Thanks for all the great write ups. You can beat any sell side analyst reports. After reading this I searched for other articles on the CLVS/EOS acquisition and did not find one that goes in as much detail and has as much substance about drug profile and market opportunity/competitors as yours.

  16. Hey Ohad
    here is the quote form Tom Davis: “Again being [indiscernible] here, TIM-1 is actually an immune modulatory protein that tumors may well use to escape the immune system, so the tumor can evade immunity, but by using an antibody or an antibody-drug conjugate, we can directly target and kill those cells as well.”

  17. Chris, now to expensive. OMED was mentioned in the past see Synta-blog: November 6, 2013 at 3:33 am

  18. Toby, Omed was mentioned, however this was before the agreement with CELG to develop and commercialize up to six anti-cancer stem cell product candidates from OMED’s biologics pipeline. OMED will receive an upfront payment of $155 million, and CELG will also purchase approximately $22.25 million in a private placement of newly issued shares at a price of $15.13 per share. Just curious to know what Ohad thinks about it and if it’s good news for STML.
    Thanks.

  19. Manish – Thanks! Glad you find this helpful.

    Alex – They are selling 2 million shares which is expected to push price lower.

    Chris/Toby – Phenomenal deal for OMED, well done! Personally I can’t a way to justify it except Celgene’s habit of paying huge money for unvalidated early technology (but scientifically fascinating).
    I don’t see any read across to STML. Unlike OMED, we know they one drug that works as monotherapy.

    Ohad

  20. Ohad
    No accelerated approval for AMBI. FDA does not accept their surrogate endpoints!
    How does it change the company evaluation? The pps after hours is $8 which corresponds to about $145M market cap. Is it fair or now too expensive (I guess 3 years P3 trail plus OS follow-up of 1 year, plus 1 year for NDA and approval – so no revenue until 2019-2020).
    Do you follow CYCC? Their Sapacitabine for AML is in Ph3 with read-out in 2014 and possible approval in 2015 They will start Ph 3 in 2014 for MDS. Market cap of CYCC is only $90M.
    thanks–andre–

  21. andre – Disappointing but the end of the world for AMBI. Quizartinib still has the highest response rate in AML (in FLT3+ patients). If anything should work in that dreadful diseases, it is quizartinib.
    Re: CYCC from what I recall their data wasn’t exciting. I wouldn’t buy ahead of results despite the tempting valuation.

    Ohad

  22. Ohad, want to take a closer look at AMBI given the sell-off. Beyond quizartinib, I see they appear to have a wholly-owned JAK2. Do you see any value in this asset given interest in the space and know of any ways in which it could be differentiated from the competition? Also, what about AC708, the CSF1R inhibitor?

  23. mcbio – They’ll have to show something really special with their JAK2 in order to be a relevant player in MF/PV imo. I am more interested in the the CSF1R program, which is a very intruguing target for immune modulation (but still no validation)

    Ohad

  24. Ohad
    Galapagos reported positive Ph1 data for GLPG1205 in inflammatory disorders.
    In the press release they call it “first-in-class molecule” but do not disclose the target.and biomarkers?!? Why they keep the target secret? It does not make any sense to me.
    –andre–

  25. Quite a drive for AMBIT! I know there are high expectations for next week but, the future seems to point to a very glumly one, disagreement with the FDA…. or is just me?
    Thoughts?
    Dan

  26. Andre- i assume they want to stall competitors as much as possible assuming glpg is the only one pursuing this target.

    Dan- i don’t think the FDA’s refusal changes a lot. Accelerated approval could be a nice bonus but the drug is clearly active and AMBI’s market cap is 150. Pretty low for an almost p3 company with a 50 response rate in a disease like AML.

    Ohad

  27. Ohad, have you ever looked at Ono as potential investment? I know you said before they have a promising BTK inhibitor on the way, albeit well behind PCYC. Still could be plenty of room for another BTK, particularly if differentiated from PCYC BTK in some way. I believe they also have full Japanese rights to nivolumab and rest of world royalties if not mistaken.

  28. Ohad
    Puma jumped to $2.2B valuation based on positive results with HER2 inhibitor.
    Why Array is not getting any credit for their 380 program? ARRY has $730M valuation and probably nothing is assigned to their selective HER2 kinase inhibitor
    –andre–

  29. Ohad
    GERN- 41% response in myelofibrosis patients, 20% total remission.
    Do these meet your expectations?
    –andre–

  30. mcbio – You are right, Ono has some great assets in its portfolio. On top of nivo and the Btk inhibitor, it also has japanese rights for Kyprolis.

    andre – The market ignores ARRY380’s potential because it is still very much “on paper” without a solid clinical proof of concept. We don’t know whether a selective HER2 inhibitor will be enough and nertainib puts a high standard.

    Re GERN, let’s wait for data presentation at ASH.

    Ohad

  31. Ohad- I established a small position in Prothena Corp.[symbol prth] in December of 2012 when they were spun out from Elan.I was impressed with not only their science but also their management.I am aware that this is not a field that you normally cover,but was hoping you could provide me with your very valued insight.

  32. Ohad
    Last year you finished with an excellent summary – Biotech portfolio 2012 summary and 2013 outlook. Personally for me it was a very helpful guide through 2013.
    Do you plan to finish this year with similar article? It would be helpful to add a list of companies which you follow closely and would potentially add to the portfolio if some specific targets are achieved.
    thanks-andre–

  33. Ohad – A lot of buzz about CAR-T at ASH this weekend. What do you think about $BLUE as a CAR-T play? There appears to be a lot of formidable competition in this area from $NVS/UPenn, Juno/MSKC/Fred Hutch, $GSK/Immunocore, etc. How competitive do you think the $CELG/$BLUE/Baylor team will be? Is it worth placing a bet on them at this early stage, or would you wait for actual data from them?

  34. sherk, not Ohad, but BLUE isn’t even going to be in the clinic with their CAR T tech partnered with CELG until 2016 as I understand. Definitely worth keeping an eye on but they have a ways to go. Also, while NVS seems to have a big lead, that is primarily only in CLL/ALL (a lot of their other CAR T stuff is pre-clinic). Not sure of exact status of some of the others.

  35. Agree, BLUE/CELG are far behind the CD19 CARs but they will probably pursue additional targets. I am actually starting to like BLUE more and more based on their other programs, the CELG collaboration is a bonus for the long term.

    Ohad

  36. It looks like BLUE is going to be going after CD34 among others, based on some of their job postings.

  37. CD34 is a marker on hematopoietic progenitor cells they collect from patients for their gene therapy programs. Don’t think that’s a target.

    Ohad

  38. Ohad,

    What did you think of the ARRY 520 data at ASH? Didn’t seem to be anything that Squarer hadn’t already telegraphed. The Market certainly doesn’t like it. I think Squarer’s registrational strategy for 520 is very misguided. Trials will be very long and expensive and the MM landscape is a moving target. I say partner the damn thing worldwide and move on. I know Squarer wants ARRY to be a hem once company, but it isn’t likely to happen.

  39. Ohad, Hey,
    is the pop and then fall of IFI today, on the good news a buying opportunity? more than 10M shares traded already. What do you think is happening?
    Thanks
    Dan

  40. Richard – ARRY-520 is stuck in the middle, it’s certainly active but not as active as other agents (CD38 abs, pomalyst, kyprolis etc.). In theory, being one of the first drugs to be combined with Kyprolis in p3 could create an opportunity the problem is that so far data don’t look that great imo. Stratifying patients based on AAG levels may provide the required edge both as monotherapy and in combination with Kyprolis.

    Ohad

  41. Hey Ohad,

    after Ambit stockprice fell 5 days ago, do you plan to add more and do you see some near term catalysts there?

    Generally: The global economy is ill, experts expect a new big crash in the upcoming years. Unfortunately the development of new drugs needs a long time. So do you see there any risks for ph1/2-companies? Do you think it’s useful to add more early stage-companies to the portfolio?

    Thank you for your answer and your great blog!

  42. Martin – Yes, I am plan on adding AMBI since I think it’s fairly cheap for an almost p3 company with clear proof of concept and a biomarker for patient selection.
    With respect to the global economy and market trends, I find it almost impossible to predict the market’s direction although in general I feel a correction is imminent (full disclosure, I thought so 6 months ago too…) especially in biotech where prices are high. This is why I try to have a large cash position.

    Steve – There were signs of activity for ARRY614 but I don’t find this program so exciting. Focus should be on other programs imo, of which there is plenty.

    Ohad

  43. Hey Ohad,

    nice post on Clovis. Just wondering what you think about the competition in mutant EGFR NSCLC. I imagine Astra will push hard with AZD9291. I like the EOS deal, but also competition among the PARP inhibitors. Just curious to hear your thoughts on how the competition will play out allowing Clovis to keep an edge in these areas. How will PD-1 development impact EGFR inhibitors overall in NSCLC? Complementary?

  44. Hi Ohad,
    Any thoughts on CYTR and their soft sarcoma update this week? Huge move this week on Phase IIb interim data.
    thanks
    Jeff

  45. Care – Regarding CLVS vs. AZN. I think it’s safe to say both drugs look active in T790M NSCLC even though it’s hard to predict the eventual clinical profiles of each drug. To me, the fact CLVS’ recruit patients only immediately after progression on Tarceva (or other EGFR inhibitor) makes their case more compelling. In addition, CLVS’ compound might be more wild type EGFR sparing based on some rast AZN reported.
    Wit respect to PD-1, I don’t view them as a threat to EGFR inhibitors as I believe the vast majority of EGFR mutated cases will be treated with EGFR inhibitors, let alone patients with a documented T790M mutation. Combination of the two classes of drugs is very likely down the road (no overlapping toxicities).

    Alex – I think they have great scientific background, a compelling story but a very limited clinical package. I still can’t get the biologic rationale for selecting patients based on merlin levels…

    andre – Yes I did but still haven’t made up my mind yet. There’s definitely something there but how strong it is, I don’t know.

    Jeff – Haven’t looked at the data thoroughly. Numbers look good but based on ZIOP’s case, I would be cautious, soft tissue sarcoma is a very heterogeneous indication.

    Ohad

  46. Ohad, SCTPF just raised $33M to take their CD47 through rest of pre-clinical development and Phase 1. Any thoughts? It was a very dilutive offering but, as a long, I’m happy with it because it beats the alternative of them partnering their CD47 for peanuts at this early stage or, worse, going bankrupt. Also good to see some bigger name U.S. investors involved in the offering.

  47. Hi Ohad, Do you follow Innate Pharma (IPHYF)? What do you think its current valuation and its programs? Thanks!

    bj

  48. Christian: Agree that is certainly a fair caveat on SCTPF. I’m waiting to hear back from the company to get a clear sense on fully-diluted share count. It’s important to know that for sure to get a sense of risk-reward going forward.

  49. Ohad, dicing the $kpti data, the response is really very short. I sold my entire position. The drug is not very useful and more to be proved later.

  50. mcbio – In these type of situations, a large dilutive financing is always better than several repetitive small rounds with the overhang of bankruptcy. In any case, the program looks still far from P1 as the press release states toxicology and CMC work that need to be done (1-2 years?).
    What is the fully diluted number of outstanding shares?

    BJ – Not following them closely but I am not too enthisiastic about them. Nevertheless, many are excited about them, including BMS, which will have combo data next year.

    Bridgette – Agree, durability wasn’t great but the drug is clearly active. The problem in today’s world that you need to have something phenomenal to compete with the new agents.

    Alex – I find INFI’s CLL data somewhat disappointing and undifferentiated from idelalisib, th iNHL response rate was high but the sample size was small and te PFS looks comparable. I liked the PTCL response rate, though. If responses there are durable enough , it could be a good near term opportunity.

    Ohad

  51. Ohad: Agree completely with you on financing for small-caps with little money. SCTPF said before they expect their CD47 to enter P1 2H’15 so a bit away but these funds should clearly get them to that point and hopefully a bit beyond. I am awaiting a response from the CFO to confirm fully-diluted share count as the numbers in the PR are a bit confusing.

  52. SSS.v fully diluted over 200 million shares. That is just to get to IND. They basically gave the company away to Americans.

  53. Ohad. The more I look at $ambi data the more I think. This drug is real and differentiated.

  54. Bridgette: Even at over 200M fully-diluted share count, that puts valuation at only about $50M (based on Friday close). Let’s see what happens to share price on Monday. I’m happy that some legitimate American players saw it worthwhile to get involved here.

    P.S. Since you are Canadian, what are your thoughts on Lorus? They are also around $50M market cap and just raised money (much smaller and less dilutive offering than SCTPF).

  55. Mr. MC. Lorus, colleague is wary of it’s history and tough indications such as AML. Worth a speculative is what she said.

  56. Thanks Bridgette. They have had a long, undistinguished history I do think and certainly very speculative, but I like that they are pursuing novel targets that few others seem to be pursuing. For example, for AML, KLF4 does seem to be an emerging AML target based on searches I’ve done (Lorus claims silencing of KLF4 is a key driver in AML) and they think their lead drug may activate it. No position, but at this small valuation and novelty of their programs, I may consider small one in the future.

  57. Ohad and mcbio, Did you guys look at the new ipo tetralogic pharmaceuticals. Any thoughts? Thank you

  58. Mike: I took a brief look at TetraLogic. Looks like primary focus is on an IAP inhibitor. If for nothing else, I will be paying close attention to them as I’m long CRIS and CRIS also has an IAP inhibitor (though I’m mainly long for the dual PI3K/HDAC inhibitor). I’d like to know fully-diluted market cap on TLOG.

  59. Ohad, have you looked at the French company AB Science? Seems to be a true one-trick pony with a drug called masitinib that’s a TKI and hits at least c-Kit, PDGR, and Lyn but what they claim differentiates the drug from other TKIs is it also hits mast cells. Any thoughts here? They have the drug in like 9 Phase 3 trials which seems crazy. I don’t think they have ever had any kind of partner (which is probably a red flag) but they still sport about a $500M or so market cap because they had some interesting Phase 2 data in GIST and pancreatic.

  60. Mike – The data so far doesn’t look compelling enough imo. In general, smac mimetics don’t look very promising because in humans they were shown to inhibiti only cIAP and not xIAP, which is more relevant. In any case, I would go with CRIS drug, which is oral and looks more effective in humans.

    mcbio – Don’t know the program very well but my impression is that this drug has been there for years without showing good clinical activity. Therefore, I am unimpressed by the broad p3 program without a compelling biologic story.

    Ohad

  61. Hi Ohad, going into 2014 which ones in your portfolio are going to have a breakthrough year potential other then exel. tx and a Happy New Year to the family the new born and you.

  62. Happy Holidays Ohad! Wish you were my neighbor and I could bring you a 6pack or go out for coffee. Thanks for such an entertaining and critically thinking blog. Happy New Year

  63. Ohad, Happy Holidays and have a healthy and prosperous New Year. And thank you very much for generously sharing your vast knowledge with us here.

    Oh yeah, do you have an opinion on KBIO?

  64. hi Ohad

    ARRY with a BoD retirement effective immediately. do you read anything into this?

    by the way have u taken a look at PGNX lately, do you see value in this company?

  65. Thank Ohad for the best source of information and collegial discussion of any investment site extant. Your gracious sharing of information and insight is truly wonderful.
    Best wishes to all in 2014.
    Jeff

  66. Richard – Thanks. I don’t see any rason to hold KBIO despite the low valuation. None of their programs have compelling data. Imo, the most interesting one is the anti-infective program with Sanofi

    Christian – I don’t think it’s significant, sorry, haven’t been following PGNX lately.

    Jeff – Thank you for the kind words.

    Will try to publish a 2013 summary/ 2014 preview on sunday.

    Ohad

  67. Hi Ohad,

    Just realized no one asked your tale on the dara combo data at ASH. Looks like 8/11 PR, which might increase to 9 or 10 w/ longer follow up? No rxn in stock price, still seems relatively cheap, no?

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