What are the expectations for this weeks conference call? Anyone think we learn more about the NSCLC clinical program?
Either way I think this is the stock to be in ahead of ASCO... The fact that we have a randomized ph2 trial (which is rare) with a decent number of patients means we are likely to see some exciting significant data reported at ASCO. Look at OGXI and KERX as comparators to see 2 exciting companies that reported randomized ph2 results.
From my experience of going to these meetings I think it would be really rare to hear anything negative reported at the LBA oral session. I believe the additional color behind the data that we hear should be a significant positive for ARQL pps. From what I understand of the company this level of clinical data should be new territory for the company (anyone see this differently?)
The fact that PFE's drug which is also a c-met inhibitor has the plenary presentation at ASCO has to draw extra excitment towards the ARQL compound.
I should note that Pfizer's drug is distinct in that it also inhibits ALK kinase (many of their trials are designed towards that mutation) and is actually an ATP competing inhibitor. The common theme of c-met inhibition leading to robust clinical activity should be getting the limelight very shortly. I can already imagine the post-ASCO press talking about both drugs together and when choosing between ARQL and PFE its clear who will be getting investors attention.
Thanks for pointing out PFE compound's cMet connection. I just looked at it, together with ARQL 197, it will definitely generate "buzz" at ASCO.
THE ROLE OF C-MET AND ALK • The c-MET proto-oncogene is a receptor tyrosine kinase which is normally activated through binding to hepatocyte growth factor (HGF). HGF-MET signaling plays a critical role in regulation of tumor oncogenic processes such as mitogenesis, survival, and invasive growth, especially in the metastatic process.1 • Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase that is normally expressed in discrete regions of the developing nervous system. 2 • Chromosomal rearrangements (translocations) that interrupt the ALK gene and fuse it with another gene result in the creation of oncogenic ALK fusion genes that enhance cell proliferation and survival. 3 RATIONALE FOR TARGETING C-MET / ALK IN CANCER • c-MET is one of the most common genetically altered tyrosine kinases in human cancers, including hereditary papillary renal cell carcinoma, lung cancers, head and neck cancers, colorectal cancer, hepatocellular and gastric cancer. 4-8 • Oncogenic mutant or fusion variants of ALK were identified in several human cancers, including non-small cell lung cancer (NSCLC), anaplastic large cell lymphomas, neuroblastomas, and myofibroblastic tumors. 3 • A subset of NSCLC was recently demonstrated to carry a translocation, in which the echinoderm microtubule-associated protein-like 4 (EML4) gene is fused to ALK, representing one of the newest molecular targets in NSCLC. 9 ABOUT PF-02341066 • PF-02341066 is a selective ATP-competitive small-molecule inhibitor of both c-MET/ HGF receptor and ALK tyrosine kinases and their oncogenic variants (e.g. mutations, fusion proteins). • PF-02341066 is currently being investigated in an open-label, dose-escalation Phase 1 study in patients with advanced solid tumors. The study also includes an expansion cohort in patients with tumors harboring c-MET amplification/gene mutation or translocation or inversion events involving the ALK gene locus (e.g. EML4-ALK, fusion variants). • PF-02341066 is the first agent in the clinic to selectively target the EML4-ALK translocation in NSCLC patients.
I have read its broad platform technology is currently undervalued. I am a relatively new arq investor and wonder why did arql rise before 2009 asco only to lose almost half its value up to early this year?