11/2/05 analyst day highlights
P 1 / 2 data V + Rev at Ash
Updated Apex survival data at Ash
V re-treatment data 2nd ½ ‘06
Mantel cell trial completed now; snda in 2nd ½ ‘06
Interim V data for relapsed follicular lymphoma at Ash
Encouraging, early SWOG P 2 front line nsclc data; V + gemcitabine + carboplatin; final data 1st ½ ‘06
2nd line nsclc P 1 / 2 V + tarceva started
2nd line nsclc P 1 / 2 V + alimta planned soon
BAC single agent P 2 ongoing
2 of the new molecules have applicability to cancer and inflammation; ccr1- - inflammation, MM and bone metastases; ikkß - - inflammation, lymphoma, myeloma, chemotherapy-resistant solid tumors
believes 02 is gut-specific and won’t see immune system turned off in other end organs
initiated P 1 with 8054, aurora A kinase oral inhibitor- - colorectal, solid and hematological tumors; uses a novel scaffold with possible applications for many other kinases
2nd generation proteasome inhibitor in clinic in 2007
0415 oral ikkß inhibitor - - preclinical activity in RA, MS, COPD; in clinic 2nd ½ 2006
data on V in ovarian and prostate cancers will be available by year end
talking to NIH about trials for V in stroke
SWOG nsclc study data will be available at asco in may
Re: competition, V has always added value in combo
Re: specificity of ccr2, might you be blocking something else? - - that’s why we wanted to try many indications early. Possible next steps- - scleroderma P 2a --> P 3; all other indications would go to P 2b next
V targets a different subset of BAC patients than tarceva and iressa; V will be active in patient population that does not require a egfr mutation
We are in the process of approving an investigator-initiated sponsored trial for V + avastin
02 is a high priority for us in UC since it has shown a clinical response in both UC and Crohn’s; dna passed on it as a portfolio decision
initiatives that will increase V sales - - adding more salespeople; adding more cycles; everest retreatment could propel sales like rituxan; front-line mm; nhl/mantel cell;nsclc
V is multiple drugs in one; V inhibits multiple mechanisms in one drug and that’s why with V we don’t see significant acquired resistance in hematological malignancies; V is a stabilizer of tumor suppressors, has anti-vegf activity, inhibits ikk through nfkb stabilization of ikb, and has an effect on cyclins
It may be that the reason that V hasn’t worked on all tumor types so far is not because V is targeting the wrong key mechanisms; rather, V may not be penetrating enough; we’re still working on this idea
Impressions:
the SWOG lung cancer data sounded good
strong presentation and discussion of r&d efforts by tepper and schenkein; did their r&d efforts just need more time?
It’s probably just a matter of time before they do another deal with jnj for 0415 and/or 2nd generation V
molecules were divided into those that were biologically active vs. those that needed proof of concept; the order presented was: V, 02, 518, 2704; and 8054, 1202, 3897 and 0415
sales
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