Anjali Pandey
Senior Vice President Medicinal Chemistry & Chemical Development, Portola Pharmaceuticals, Inc
ANJALI PANDEY, Ph.D.
Senior Vice President, Medicinal Chemistry and Chemical Development
Senior Vice President, Medicinal Chemistry and Chemical Development
Dr. Anjali Pandey joined Portola in November 2003 and has served as senior vice president of medicinal chemistry and chemical development since July 2015 and vice president chemistry since April 2006. Dr. Pandey is responsible for the overall leadership of medicinal chemistry, process research and development, manufacturing of active pharmaceutical ingredient and drug products for clinical candidates. Dr. Pandey is leading clinical and development efforts for Portola’s oral, dual Syk-JAK kinase inhibitor cerdulatinib, and development of Portola’s intellectual property portfolio. Prior to Portola, she held senior research positions at Millennium Pharmaceuticals and COR Therapeutics. Dr. Pandey has over 20 years of biotechnology experience with hands-on involvement in all stages of drug development, from initial lead identification to Phase 3 clinical trials. Dr. Pandey is the principal inventor of cerdulatinib, the Syk-selective inhibitor PRT2607, and the flt-3 receptor tyrosine kinase inhibitor tandutinib. She played a key role in the discovery and development of Portola’s Factor Xa inhibitor betrixaban and the P2Y12 receptor antagonist elinogrel. Dr. Pandey has published over 30 scientific publications and reviews and is co-inventor on 40 issued U.S. patents and 30 U.S. patent applications. She holds an M.S. from the Indian Institute of Technology in Kanpur, India, and a Ph.D. from Southern Illinois University. Dr. Pandey completed her postdoctoral fellowship in bioorganic chemistry at SRI International (formerly Stanford Research Institute).
Background*
Dr. Anjali Pandey, Ph.D. has been Senior Vice President of Medicinal Chemistry & Chemical Development at Portola Pharmaceuticals, Inc. since August 5, 2015. Dr. Pandey served as a Vice President of Chemistry at Portola Pharmaceuticals, Inc since April 2006 until August 5, 2015. Dr. Pandey served as Vice President of Medical Chemistry at Portola Pharmaceuticals, Inc. Ms. Pandey joined Portola in 2003. Ms. Pandey served as the Director of Chemistry at Millennium. She also
links https://www.linkedin.com/in/anjali-pandey-587b9a
links https://www.linkedin.com/in/anjali-pandey-587b9a
Experience
Senior Vice President, Medicinal Chemistry & Chemical Development
Portola Pharmaceuticals, Inc
Twenty years of biopharmaceutical industry experience with in-depth involvement in all stages of drug discovery and development, from initial lead identification to Phase III clinical trials. Led multiple programs from initiation through first-in-man studies, made significant contributions to research activities related to lead identification, optimization, and selection of clinical candidates. Demonstrated strong scientific leadership, insights, know-how, and creativity in medicinal chemistry programs. Extensive experience in providing overall leadership to process research and development, outsourcing and discovery collaborations. Demonstrated ability to successfully deliver on discovery to manufacturing projects, partnering with global contract manufacturing organizations for API and Drug Product. Well versed in cGMP and CMC. Supervised the development and management of Portola’s intellectual property portfolio. Provided leadership role in IP due diligence analysis associated with S-1 filing for the IPO, subsequent offering and partnering discussions. As head of the department and member of the management team, have significant experience in in-house decision making and corporate partner interactions.
Senior Director, Medicinal Chemistry
Portola Pharmaceuticals, Inc
-Played a leading role in discovery and development of an orally bioavailable, reversible and potent P2Y12 receptor antagonist, Elinogrel (Phase II Clinical Trial completed, Partnered with Novartis)
-Responsible and supported the development of Factor Xa inhibitor.betrixaban (Phase II SPAF trial completed)
•Managed and directed the medicinal chemistry efforts towards identification and characterization of structurally distinct orally bioavailable and once a day backup Factor Xa inhibitor.
•Principal inventor and key contributor in the discovery and preclinical development of a once a day, orally bioavailable and potent Flt-3 (receptor tyrosine kinase inhibitor), Tandutinib (MLN518) in Phase II for Acute Myelogenous Leukemia (AML).
•Key inventor of orally bioavailable platelet derived growth factor receptor antagonist, MLN608 (Preclinical).
•Played a key role in discovery and development of 2nd Generation Oral GPIIb-IIIa antagonist clinical candidate CT51464 (on hold) with better pharmacokinetics properties (F% & T1/2) than other inhibitors in clinical trials.
-Responsible and supported the development of Factor Xa inhibitor.betrixaban (Phase II SPAF trial completed)
•Managed and directed the medicinal chemistry efforts towards identification and characterization of structurally distinct orally bioavailable and once a day backup Factor Xa inhibitor.
•Principal inventor and key contributor in the discovery and preclinical development of a once a day, orally bioavailable and potent Flt-3 (receptor tyrosine kinase inhibitor), Tandutinib (MLN518) in Phase II for Acute Myelogenous Leukemia (AML).
•Key inventor of orally bioavailable platelet derived growth factor receptor antagonist, MLN608 (Preclinical).
•Played a key role in discovery and development of 2nd Generation Oral GPIIb-IIIa antagonist clinical candidate CT51464 (on hold) with better pharmacokinetics properties (F% & T1/2) than other inhibitors in clinical trials.
Education
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| AML FIGHTERPandey, shown in her lab at Millennium, helped develop an acute myelogenous leukemia agent.MILLENNIUM PHARMACEUTICALS PHOTO |
Anjali Pandey, director of cardiovascular chemistry at Millennium Pharmaceuticals, South San Francisco, reported on CT53518 (also known as MLN518), a potent, orally available inhibitor of the enzyme FLT-3. The drug is a potential therapy for acute myelogenous leukemia (AML), a form of cancer in which abnormal white blood cells accumulate in the blood and bone marrow, resulting in hemorrhage, fatigue, and other symptoms.
FLT-3 is a receptor tyrosine kinase (a tyrosine kinase found in cell membranes) and a member of the platelet-derived growth factor receptor (PDGFR) family of enzymes. These cell-signaling enzymes have been implicated in a variety of cancers and other diseases and are a major focus of current drug discovery efforts.
"Kinase inhibition represents a novel mechanism-based approach to selectively block cell-signaling pathways," Pandey said. "This strategy has been validated recently by the introduction of the Bcr-Abl kinase inhibitor Gleevec for chronic myeloid leukemia" (CML). Gleevec is a Novartis drug that prevents activation of Bcr-Abl, the abnormal nonreceptor tyrosine kinase that causes CML.
More than one-quarter of AML patients have internal duplications in FLT-3 that cause the enzyme to be activated inappropriately and that are associated with significant increases in relapse and mortality rates. Inhibiting FLT-3 could help ameliorate AML symptoms in such patients.
Pandey and coworkers at Millennium began their project by identifying a quinazoline class of compounds as leads for FLT-3 inhibitors in a high-throughput screening procedure. Pandey noted that, in the past, the quinazolines have been a prolific source of tyrosine kinase inhibitors, such as ZD1839 (Iressa) and OSI-774 (Tarceva), which are in Phase III and Phase II clinical trials for cancer, respectively. ZD1839 is an AstraZeneca drug; OSI-774 is being codeveloped by OSI Pharmaceuticals, Genentech, and Roche.
The original quinazolines identified by Pandey and coworkers had instability, potency, and aqueous solubility problems. So the researchers synthesized a range of variants, analyzed SAR data on these compounds, and further modified their structures to zero in on agents with optimal in vitro potency and physicochemical properties. They narrowed the field to four compounds, tested them in animals, and chose CT53518 (MLN518) as a clinical candidate for further characterization.
The group found that the drug delayed disease progression in a mouse model of FLT-3-associated AML and caused apoptosis (cell death) in a human AML cell line. "We have done 28-day toxicological tests in rat and dog, and it looks pretty good," Pandey said--except for some slight suppression of bone marrow, which she and her coworkers had expected. "Phase I clinical trials in AML patients have been initiated," she said, "and we are very hopeful" that results will continue to be favorable.
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