INmune Bio Inc. Demonstrates that INB03 Enhances the Uptake of Trastuzumab Deruxtecan in HER2+ Breast Cancer with MUC4 Expression in Poster Presented at San Antonio Breast Cancer Symposium
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INmune Bio Inc. Demonstrates that INB03 Enhances the Uptake of Trastuzumab Deruxtecan in HER2+ Breast Cancer with MUC4 Expression in Poster Presented at San Antonio Breast Cancer Symposium

INmune Bio, Inc.
INmune Bio, Inc.

INB03 increases uptake of deruxtecan, the immunotoxin associated with trastuzumab deruxtecan (T-DXd, ENHERTU®), in models of resistant MUC4 expressing HER2 positive breast cancer and increases the tumor killing immunology of the tumor microenvironment.

Boca Raton, Florida, Nov. 29, 2023 (GLOBE NEWSWIRE) --  INmune Bio, Inc. (NASDAQ: INMB) (the “Company”), a clinical-stage immunology company focused on developing treatments that harness the patient’s innate immune system to fight disease, is presenting data on the use of INB03, a dominant-negative TNF inhibitor of soluble TNF (sTNF) in the treatment of high-risk MUC4 expressing HER2. Roxana Schillaci, Ph.D., of Instituto de Biología y Medicina Experimental in Buenos Aries, Argentina, will present her work at the 46th annual San Antonio Breast Cancer Symposium, which runs from December 5 to 9.

“This work demonstrates another way that MUC4 expression causes resistance to HER2-targeted immunotherapy in women with resistant breast cancer," said Dr. Schillaci, who is also associated with CONICET and is senior author of this work. “MUC4 expression decreases the uptake of the antibody-drug conjugate T-DXd. Decreased T-DXd uptake results in less tumor killing in this tumor model and we suspect it plays an important role in relapse of disease after treatment with T-DXd.”

The poster, titled, “Blocking soluble TNF to improve potency of trastuzumab-deruxtecan by increasing internalization and antitumor innate immune response in a resistant HER2-positive breast cancer model, shows that INB03 improves the potency of T-DXd in a model of immunotherapy resistant HER2+ breast cancer. INB03 decreases resistance to T-DXd therapy in three ways. INB03 decreases MUC4 expression on the surface of the breast cancer cells increasing the ability of the antibody to bind to the HER2 target on the cancer cell. The combination of low-dose (1.5mg/kg) T-DXd+INB03 decreases tumor growth as much as full dose (5mg/kg) T-DXd alone suggesting increased binding of the immunotoxin to the cancer cell improves anti-tumor effects. INB03 increases internalization of T-DXd and converts the immunosuppressive TME into one that is more tumor-sensitive by polarizing tumor associated macrophages (TAM) from M2-like to M1-like phenotype with increased expression of IFNg. The poster concludes that the combination of INB03 may allow for lower doses of T-DXd to be effective in women with MUC4 expressing HER2+ breast cancer and that addition of INB03 may improve the response to T-DXd in women with resistant HER2+ disease.