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SUMMARY:Leveraging PROTACs to Overcome Resistance in Targeted Cancer Thera
 pies and Immunotherapies
DTSTART:20220520T140000
DTEND:20220520T150000
DTSTAMP:20260506T015731Z
UID:45ec16b47b5e68bd3213e885a5b063d7164d69ec3c1a6858d500b0d6
CATEGORIES:Conferences - Seminars
DESCRIPTION:Jin Wang\, Ph.D.\nMichael E. DeBakey\, M.D.\, Professor in Pha
 rmacology and CPRIT Scholar\nDepartment of Pharmacology and Chemical Biolo
 gy\nBaylor College of Medicine\nHouston\, TX 77030\n \nAbstract\nPROTACs 
 are a novel therapeutic modality to inhibit the scaffolding functions of p
 roteins. I will discuss our work on the first reversible covalent PROTAC t
 argeting Bruton’s Tyrosine Kinase (BTK) (Nature Communications 2020). Se
 rendipitously\, we discovered that cyano-acrylamide-based reversible coval
 ent chemistry can significantly enhance the intracellular accumulation and
  target engagement of PROTACs and developed RC-1 as a reversible covalent 
 BTK PROTAC with a high target occupancy as its corresponding kinase inhibi
 tor and effectiveness as a dual functional inhibitor and degrader\, provid
 ing a novel mechanism-of-action for PROTACs. Additionally\, I will present
  our recent work on a novel PROTAC to boost antitumor immunities of cancer
  immunotherapies. One common feature for immune checkpoint blockades (ICBs
 )\, activated cytotoxic T cells\, CAR-T and CAR NK cells is that they all 
 kill cancer cells through granule exocytosis and death ligands to activate
  programmed cell death. However\, cancer cells that are insensitive to the
 se programed death mechanisms will evade killing mediated by the antitumor
  immunity. We developed a novel PROTAC that can synergize with anti-PD1 to
  trigger immunogenic cell death and significantly inhibit tumor growth in 
 an immunotherapy insensitive B16F10 mouse melanoma mouse model.\n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717 https://epfl.zoom.u
 s/j/61177102929?pwd=QUo2OGdtRUEvVkZCTC9ZUU90akRnQT09
STATUS:CONFIRMED
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