On April 10, 2018 Asana BioSciences, LLC, an oncology focused, clinical stage biopharmaceutical company, reported that it will present updates for two of its lead molecules in clinical development at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting being held in Chicago, IL, April 14-18, 2018 (Press release, Asana BioSciences, APR 10, 2018, View Source [SID1234525253]).

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The presentation details are as follows:

1. ASN003, a novel highly selective BRAF and PI3K dual inhibitor: Phase I PK/PD results in patients with advanced solid tumors.

Authors: D. Rasco1, N. Lakhani2, R. Sullivan3, M. Mita4, J. Shah5, H. Usansky5, S. Reddy5, N. S. Rao5, L. Denis5, K. Flaherty3, Anthony Tolcher6. 1START Med. Oncology, San Antonio, TX; 2START Med. Oncology, Grand Rapids, MI; 3MGH, Boston, MA; 4Cedars Sinai Med. Oncology, Los Angeles, CA; 5Asana BioSciences, Lawrenceville, NJ, 6NEXT Oncology, San Antonio, TX.
Session: PO.CT01 – Phase I Clinical Trials 1; Section 42
Abstract: #CT019 / 12
Date/Time: Sunday, April 15 at 1:00pm – 5:00pm

2. Strong antitumor activity of ASN007, an oral ERK1/2 inhibitor, in PDX tumor models with MAP kinase pathway alterations including KRAS mutations.

Authors: Sanjeeva P. Reddy, Niranjan S. Rao, Roger A. Smith, Scott K. Thompson, Sarper
Toker. Asana BioSciences, Lawrenceville, NJ.
Session: PO.ET06.10 – Canonical Targets 2; Section 36
Abstract: #5783 / 9
Date/Time: Wednesday, April 18 at 8:00am – 12:00pm

ASN003 is a potent and highly selective inhibitor of both B-RAF and PI3 kinases. RAS-RAF-MEK and PI3K-AKT-mTOR are two major pathways involved in tumor cell signaling and growth. Components of these pathways are frequently mutated in a broad range of tumors. Selective BRAF inhibitors induce dimerization of RAF proteins, leading to paradoxical activation of the RAF-MEK-ERK cascade. This activation is a major limitation for the clinical use of selective RAF inhibitors, as it leads to resistance and results in side effects in the skin limiting their use in patients with BRAF mutant tumors. In addition, elevated signaling through the PI3K/AKT pathway, with or without concomitant MAPK reactivation, represents an alternative path to resistance to BRAF inhibitors. ASN003 demonstrates broad anti-proliferative activity in tumor cell lines and strong tumor growth inhibition in tumor xenograft models, including BRAF inhibitor resistant models. ASN003 is currently in Phase I clinical development in patients with advanced solid tumors, including melanoma, colorectal cancer and non-small cell lung cancer (clinicaltrials.gov NCT02961283). ASN003 is well tolerated and shows the potential to be developed as a monotherapy or in combination with checkpoint inhibitors or other standard of care.

ASN007 is a potent inhibitor of the extracellular-signal-regulated kinases, ERK1 and ERK2 (ERK1/2), key players in the RAS/RAF/MEK (MAPK) signaling pathway. This pathway is frequently hyper-activated in a wide range of cancers through mutations in upstream targets such as BRAF and RAS proteins. Inhibition of ERK1/2 offers a promising therapeutic strategy for such cancers. ASN007 shows potent and selective anti-proliferative activity in cancer cell lines that are driven by the MAPK-pathway, including RAS mutant cell lines. Furthermore, ASN007 demonstrates strong inhibition of tumor growth in multiple BRAF and KRAS mutant patient-derived and cell-line-derived xenograft models, including those that are resistant to BRAF and MEK inhibitors. ASN007 is currently in Phase I clinical development in patients with advanced solid tumors, including melanoma, colorectal cancer, non-small cell lung cancer and pancreatic cancer (clinicaltrials.gov NCT03415126).