P2, N=100, Recruiting, University of Pennsylvania | Trial completion date: Aug 2027 --> Dec 2028 | Trial primary completion date: Feb 2026 --> Oct 2027

P3, N=120, Not yet recruiting, SDK Therapeutics, Inc.

P2, N=100, Recruiting, University of Pennsylvania | Not yet recruiting --> Recruiting

P1, N=12, Completed, SDK Therapeutics, Inc. | Phase classification: P1/2 --> P1

P2, N=100, Not yet recruiting, University of Pennsylvania

P2, N=27, Recruiting, Abramson Cancer Center at Penn Medicine | Not yet recruiting --> Recruiting

Our study provides insights into the specific delivery of hAFSC-EVs into inflammatory macrophages and sheds light on the potential therapeutic applications of these EVs for regulating inflammatory macrophage phenotypes.

Notably, in vivo experiments illustrated the efficacy of baicalin-PMs in suppressing M1 macrophage polarization and restraining tumor growth in the context of Lenvatinib resistance in ATC. Overall, the comprehensive multi-omics analysis underlines the potential of baicalin-PMs in reversing Lenvatinib resistance by modulating M1 macrophage function and inhibiting the MET factor, thus offering a novel strategy and target for combatting ATC resistance to Lenvatinib.

The underlying metabolic and molecular mechanisms revealed that MICA in tumor cells induced M2-like polarization through the PPAR/EHHADH pathway, which regulates the fatty acid oxidation (FAO) in macrophages. The metabolic gene EHHADH, which is associated with MICA, led to alterations in M2-like macrophages by promoting heightened fatty acid uptake and augmenting levels of FAO within macrophages.

P2, N=27, Not yet recruiting, Abramson Cancer Center at Penn Medicine

P1/2, N=12, Completed, SDK Therapeutics, Inc. | Recruiting --> Completed

MMRN1 is a critical BTSC-related biomarker that contributes to GBM progression by enhancing tumor stemness and modulating the immune microenvironment. Targeting MMRN1 May represent a promising therapeutic approach for GBM treatment.