On March 8, 2022 Bolt Biotherapeutics (Nasdaq: BOLT), a clinical-stage biotechnology company pioneering a new class of immuno-oncology therapeutics that combine the targeting precision of antibodies with the power of both the innate and adaptive immune systems, reported that it will present posters for three of the company’s preclinical pipeline programs at the upcoming American Association of Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022, being held in-person and virtually at the Ernest N. Morial Convention Center in New Orleans, LA from April 8-13, 2022 (Press release, Bolt Biotherapeutics, MAR 8, 2022, View Source [SID1234618689]).
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"We are pleased to present three poster presentations at the AACR (Free AACR Whitepaper) Annual Meeting that highlight the significant progress made by our research team and the depth of our expertise in myeloid biology. We are continuing to expand our Boltbody ISAC platform with advanced CEA- and PD-L1-targeting ISACs, both of which have the potential to provide cancer patients with new options where few treatments are currently available. We are expanding our pipeline beyond ISACs through the development of our novel myeloid modulating antibody, BDC-3042, which repolarizes tumor-associated macrophages, or TAMs, into tumor destructive macrophages via agonism of Dectin-2," said Randall Schatzman, Ph.D., Chief Executive Officer of Bolt Biotherapeutics.
Three of Bolt Biotherapeutics’ preclinical programs will be featured in poster presentations: (1) BDC-2034, a CEA-targeting immune-stimulating antibody conjugate (ISAC) expected to enter clinical development in the second half of 2022, (2) BDC-3042, a Dectin-2-targeting, myeloid-modulating antibody anticipated to enter clinical development in 2023, and (3) a PD-L1-targeting ISAC. These posters will highlight updates on preclinical research for each of the programs, demonstrating anti-tumor activity and supporting future clinical development for all three programs.
Poster presentation sessions will be conducted in-person and available electronically on April 12 and 13 and will be published in Proceedings of the AACR (Free AACR Whitepaper). Details for each presentation can be seen below and on the AACR (Free AACR Whitepaper) website.
Title: The CEA-targeted ISAC, BDC-2034, shows preclinical efficacy associated with innate immune activation, phagocytosis, and myeloid reprogramming
Presenter: William G. Mallet, Ph.D.
Session Date and Time: Tuesday Apr 12, 2022, 9:00 a.m. – 12:30 p.m. CST
Location: New Orleans Convention Center, Exhibit Halls D-H, Poster Section 38
Poster Board Number: 26
Abstract Number: 2911
Title: Dectin-2 agonist antibodies reprogram tumor-associated macrophages to drive anti-tumor immunity
Presenter: Shelley Ackerman, Ph.D.
Session Date and Time: Tuesday Apr 12, 2022, 9:00 a.m. – 12:30 p.m. CST
Location: New Orleans Convention Center, Exhibit Halls D-H, Poster Section 37
Poster Board Number: 26
Abstract Number: 2883
Title: PD-L1-targeted ISAC combines myeloid cell activation, immune-checkpoint inhibition and ADCP to improve anti-tumor efficacy over anti-PD-L1 antibodies in preclinical models
Presenter: Justin Kenkel, Ph.D.
Session Date and Time: Wednesday Apr 13, 2022, 9:00 a.m. – 12:30 p.m. CST
Location: New Orleans Convention Center, Exhibit Halls D-H, Poster Section 39
Poster Board Number: 11
Abstract Number: 4252
About the Boltbody Immune-Stimulating Antibody Conjugate (ISAC) Platform
ISACs are a new category of immunotherapy that combines the precision of antibody targeting with the strength of the innate and adaptive immune systems. Boltbody ISACs comprise three primary components: a tumor-targeting antibody, a non-cleavable linker, and a proprietary immune stimulant to activate the patient’s innate immune system. By initially targeting a single marker on the surface of a patient’s tumor cells, an ISAC can create a new immune response by activating and recruiting myeloid cells. The activated myeloid cells start a feed-forward loop by releasing cytokines and chemokines, chemical signals that attract other immune cells and lower the activation threshold for an immune response. This reprograms the tumor microenvironment and invokes an adaptive immune response that targets the tumor, which can lead to the conversion of immunologically "cold" tumors to "hot" tumors with the goal of durable responses for patients with cancer.