One of the surprising things I learned over the summer was how many people misunderstand how advanced ovarian cancer is treated as a disease… it isn’t really one disease to start with, but is actually a series of subsets depending on the molecular underpinnings and also how women with the condition react to therapy.
Imagine then, when we see a series of press releases and abstracts emerge on PARP inhibitors followed by a rather indecent and sudden rush to judgment by Wall St and investors on the ‘Winner takes All’ out of the lot?
Except that real life doesn’t work that way in clinical practice.
A head/desk moment to be sure, and a frustrating one for those who understand what this is actually all about. To address this siituation, we had the pleasure of communicating with KOLs remotely or sitting down with several thought leaders in gynecologic cancer in Copenhagen to debate various aspects relating to current treatment paradigms, new clinical trial data with PARPs, and what they are most excited about going forward.
Today’s post highlights our latest thought leader interview with an experienced GYN oncologist and their perspectives on the rucaparib and niraparib data presented earlier this month at ESMO.
To learn more about their practical no-nonsense insights, Subscribers can log-in or you can sign up in the blue box below…
Today’s news that an FDA Oncologic Drugs Advisory Committee (ODAC) review will not be required for rucaparib is good news for Clovis Oncology. The company announced this via an SEC 8K filing:
“The Food and Drug Administration (“FDA”) has notified Clovis Oncology, Inc. that FDA is not currently planning to hold an advisory committee meeting to discuss the Company’s New Drug Application for rucaparib.”
However, given the unmet medical need in ovarian cancer, a lot of companies are targeting both platinum sensitive and platinum resistant disease.
In our fourth preview of the forthcoming European Society for Medical Oncology (#ESMO16) meeting we’re looking at 9 key ovarian cancer abstracts to watch out for at ESMO.
Subscribers can login to read more or you can purchase access below.
Tesaro’s niraparib is a highly selective poly(ADP-ribose) polymerase (PARP) 1/2 inhibitor that can induce synthetic lethality in tumor cells with homologous recombination DNA repair deficiencies (HRD), including germline BRCA-mutated tumours. It received a lot of attention yesterday following the company’s announcement that the phase 3 trial successfully met its primary endpoint. The trial was expected to readout this month, so it was bang on schedule.
Braving the scrum in the ASCO 2016 poster hall
The results generated a lot of discussion and also a bunch (half a dozen!) of questions from readers, since there was a lot noise around the top-line data in the press release, but very little real analysis or context.
I was planning on rolling out the draft posts we have been working on Gems from the Poster Halls, which included one focused on ovarian cancer. It therefore makes sense to combine the poster analysis with a reader Q&A on ovarian cancer, including a detailed look at Tesaro’s niraparib as there are some important subtleties that many have missed.
Inevitably this ended up as a rather meaty analysis rather than the quick review I originally intended!
To learn more about the latest developments in PARP inhibitors and the ovarian cancer landscape, you can sign-in or sign-up in the box below…
PARP inhibitors have had a chequered history as anti-cancer agents from the lows of the failed iniparib (Sanofi) phase 3 trial in triple negative breast cancer (TNBC) and olaparib (AstraZeneca) in ovarian cancer to the highs of the initial waterfall plots for BMN673 (Biomarin) in BRCA-positive breast and ovarian cancers and a successful graduation from the ISPY2 trial in the triple negative signature for veliparib (AbbVie). In between those two extremes, there has been a lot of uncertainty.
At ASCO this year, there was a decent crop of new combination data in both posters and oral sessions looking at various PARP inhibitors in breast or high grade serous ovarian cancer with either chemotherapy (typically platinum-based) or targeted therapies such as PI3K (BKM120) or VEGF (cediranib).
Another new development, which was hinted at from previous AACR conference notes was the potential to explore Biomarin’s BMN673 in lung cancer, specifically metastatic small-cell lung cancer (SCLC) and germline BRCA-mutation carrier cancer patients in a poster for a phase 1 dose finding trial.
Wainberg et al., concluded that:
“BMN 673 has antitumor activity in patients with advanced previously treated SCLC and significant activity in patients with gBRCA mut ovarian and breast cancer.”
Emphasis the authors.
For today’s article, we’re taking a slightly different approach. Rather than analyse the clinical data, I wanted to explore physician sentiments around PARP inhibitors and they thought about this class of drug. Is there still traction here or has the rise of immuno-oncology wiped out interest in targeted agents?
To find out more about the thought leader sentiments, you can sign in or sign up below: