AIM ImmunoTech Announces the Presentation of Ampligen Oncology Data at the Recent Annual Meeting of the American Association of Immunologists

On May 8, 2025 AIM ImmunoTech Inc. (NYSE American: AIM) (OTC Pink: AIMI) ("AIM" or the "Company") reported the presentation of clinical trial data involving AIM’s drug Ampligen by Pawel Kalinski, MD, PhD, at the recent Annual Meeting of the American Association of Immunologists held May 3-7, 2025, in Honolulu, HI (Press release, AIM ImmunoTech, MAY 8, 2025, View Source [SID1234652718]).

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!

The paper, titled "Systemic Infusion of dsRNA (Rintatolimod) plus IFN Promotes Selective Influx of CTLs (but not Treg) into the TME – Counteracting Chemokine Heterogeneity of the TME," discussed the unique two-level selectivity of action of Ampligen when used as a part of chemokine modulation and combined with PD-1 blockade or chemotherapy. Dr. Kalinski discussed the preclinical data and data from recently completed clinical trials showing the ability of Ampligen to selectively induce the desirable CTL-attracting chemokines, but not the counterproductive Treg-attracting chemokines, which differentiated it from poly-I:C. The second level of selectivity was the preferential activation of cancer tissues, rather than healthy tissues. The mechanistic data discussed by Dr. Kalinski indicate that the selectivity of Ampligen’s impact on the tumor microenvironment result from its avoidance of helicase-dependent activation of NFkB. This allows Ampligen to avoid the induction of TNFα and other NFkB-dependent undesirable inflammatory and suppressive factors, which are commonly induced by poly-I:C and other TLR ligands, and to focus its impact on the tumor tissues, which display elevated levels of endogenous NFkB.

AIM CEO Thomas K. Equels commented: "These findings and Dr. Kalinski’s analysis further support our belief in the potential of Ampligen as a powerful therapeutic for unmet medical needs, including deadly cancers."