On June 16, 2022 Pionyr Immunotherapeutics, Inc., a company developing first-in-class Myeloid Tuning antibody therapeutics that enhance the body’s anti-tumor immunity by altering, or "tuning," immune cells within the tumor microenvironment, reported that Chief Medical Officer Leonard Reyno, M.D., will lead a discussion on myeloid cell targeting to reprogram the tumor microenvironment, modulate innate immune activity, and enhance anti-tumor immunity (Press release, Pionyr Immunotherapeutics, JUN 16, 2022, View Source [SID1234616049]). The presentation will highlight preclinical and early clinical research on Pionyr’s first in class TREM1-targeting monoclonal antibody called PY159. The presentation titled, "Reprogramming TREM1+ Myeloid Cells to Overcome Immunotherapy Resistance in Solid Tumors," takes place at the 2nd Tumor Myeloid Directed Therapies Summit on June 16, 2022.
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"Pionyr was built on the premise that the myeloid compartment is a source of provocative, untapped anti-tumor drug targets that can be harnessed to modulate the innate immunity and our natural defenses against cancer cells," said Leonard Reyno, M.D., Chief Medical Officer at Pionyr. "With first-in-class drug candidates in clinical development targeting TREM1 and TREM2 associated myeloid cells, and a preclinical program targeting MARCO, our approach demonstrates the incredible potential to improve innate immunity, overcome the limitations of checkpoint inhibitors, and illustrate a foundational approach to transforming immuno-oncology."
As part of the presentation, Pionyr will highlight the PY159 development program. PY159 is a humanized monoclonal antibody that specifically binds triggering receptor expressed on myeloid cells 1 (TREM1). The presentation will highlight:
Preclinical research demonstrating expression of TREM1 to be higher in cancerous tissues vs normal tissues
Preclinical evidence showing TREM1 as a promising therapeutic opportunity for patients with checkpoint inhibitor (CPI)-hypo-responsive or resistant tumors as the receptor is expressed on the three myeloid immuno-suppressive cell populations
In vivo model data demonstrating administration of PY159 alone or in combination with CPIs resulted in complete regressions of tumors
First in human clinical experience administering PY159 both alone and in combination with pembrolizumab including identification of target archival tumor specimens from participating patients
Outline clinical plans for further study in patients with advanced refractory solid tumors
The Tumor Myeloid-Directed Therapies Summit is the only industry-focused meeting dedicated to unlocking novel therapeutic potential of the myeloid compartment where experts come together to identify, validate and clinically progress myeloid targets to expand the oncologist’s toolkit and realize better responses by engaging myeloid anti-tumor function. It is designed for experts working directly in myeloid-directed therapies, and those in adjacent immune-oncology fields, from cell therapy to checkpoint inhibitor development.
About Myeloid Tuning
Pionyr has developed a therapeutic platform called Myeloid Tuning, a process that rebalances the tumor microenvironment (TME) to promote anti-tumor immunity. Myeloid cells are a type of immune cell and are part of a family of cell types that play an important role in both the activation and suppression of the immune response to cancer.
One such critical type of myeloid cell, tumor-associated macrophages (TAM), are a key component of the TME. TAMs are generally categorized into two functionally contrasting subtypes called M1-like and M2-like macrophages: M1-like typically exerts anti-tumor functions, including directly mediating antibody-dependent cell-mediated cytotoxicity (ADCC) to kill tumor cells; M2-like macrophages can promote the occurrence and metastasis of tumor cells, inhibit T cell-mediated anti-tumor immune response, promote tumor angiogenesis and lead to tumor progression.
Myeloid Tuning effectively describes the mechanism of introducing agents that shift the balance of inhibitory myeloid cells – including M2-like TAMs – towards more inflammatory M1-like TAMs to promote anti-tumor immune responses in the TME and destroy solid tumors.