Dr. Bernard is a leading research biochemist and enzymologist with 16 years of experience in pharma/biotech industry. His areas of expertise include nucleotide metabolism, nucleic acids and enzymology. In large pharma (Pfizer, Bayer) and startups, Dr. Bernard’s research involved drug discovery and mechanism of action for biopharmaceuticals and small molecules in oncology, immunology and hematology. At the Pfizer Oligonucleotide Therapeutics Unit, he invented an enzymatic platform to optimize therapeutic RNA interference molecules and provide mechanistic insight. Bringing his RNAi expertise to Harvard Medical School, he discovered that HIV encodes novel microRNAs that stimulate a pro-inflammatory response through an unconventional mechanism. At Targeted Molecules Corp., Dr. Bernard initiated the program for anti-inflammatory Vatelizumab taking the program from proposal and drug discovery through humanization leading to IND. Vatelizumab completed Phase II clinical trials (Sanofi/Glenmark, $613M deal). In biotechnology, he led enzymology research at the startup Omniome to produce an enzymatic platform for label-free Next-Gen Sequencing, and at SmithKline Beckman/Beckman Instruments he produced 11 marketed IVD products. He earned degrees from the University of California, Los Angeles (B.S. Biochemistry) and Oregon State University (Ph.D. Biochemistry and Biophysics) followed by post-doctoral research at University of Texas Medical School (Medical Genetics) and Harvard Medical School (HIV and host defense). He has 10 peer-reviewed publications, 6 Patents issued/pending and prior experience at 2 startups.
Dr. Souvenir Tachado is an immunologist and research leader with over 25 years experience in academia. His areas of expertise include infectious disease, signal transduction, immunology, and cell biology. As a faculty at Harvard Medical School, he directed scientific projects in understanding why asymptomatic HIV-infected patients with reconstituted CD4+ T-cells, on highly active anti-retroviral therapy (HAART), and aviremic are susceptible to pulmonary infections. His team demonstrated that Toll-Like Receptor 4 (TLR4) signaling is significantly impaired, and impaired TLR4 signaling can be restored by immune modulation in HIV-infected alveolar macrophages. He has over 40 peer-reviewed publications.