On April 15, 2021Transcenta Holding Limited (Transcenta), a clinical stage global biotherapeutics company with fully-integrated capabilities in discovery, development and manufacturing of antibody-based therapeutics, reported that preclinical data of TST005, a bi-functional anti-PD-L1 and TGF-β trap fusion protein, in a poster during the 2021 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Virtual Annual Meeting, being held from April 10th to 15th and May 17th to 21st (Press release, Transcenta, APR 15, 2021, View Source [SID1234578100]).

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Title:
The preclinical characterization of TST005, a bi-functional anti-PD-L1 and TGF-β trap fusion protein

Abstract Number: 972
Poster Number: 917

Session Category:
Antibody Technologies

Session Title:
Experimental and Molecular Therapeutics

Poster launch time:
April 10th, 2021, 8:30 a.m.ET, U.S. time

About TST005
TST005, is a bi-functional anti-PD-L1 and TGF-β trap fusion protein designed to simultaneously target two immuno-suppressive pathways, transforming growth factor β-(TGF-β) and programmed cell death ligand-1 (PD-L1), that are commonly used by cancer cells to evade the immune system. TST005 consists of a high affinity PD-L1 antibody fused with an engineered TGF-β Receptor Type II protein in its C-terminal. TST005 lacks FcR binding and has reduced risk of FcR mediated killing of PD-L1 expressing effector T cells. TST005’s PD-L1 high binding activity and enhanced TGF-β trap stability enables the targeted delivery of TGF-β trap into PD-L1 expressing tumors, thereby minimizing off-target toxicities of systemic inhibition of TGF-β signaling. TST005 displayed potent activity in vitro in reversing TGF-β induced T-cell suppression. In multiple syngeneic tumor models, TST005 induced significant increase of CD8 T-cell infiltration into PD-L1 expressing tumors and displayed dose-dependent tumor growth inhibition. TST005 is well tolerated in non-human primates and displayed a linear PK profile. TST005 is a potential novel bi-functional immunotherapy candidate with improved therapeutic window.