P2, N=35, Not yet recruiting, Second Affiliated Hospital, School of Medicine, Zhejiang University

P2, N=60, Recruiting, Incyte Corporation | Not yet recruiting --> Recruiting

P4, N=350, Not yet recruiting, Shanghai Zhongshan Hospital

Exploratory analysis indicates that responders show significantly higher tumor PD-L1 expression than non-responders do, with median tumor proportion scores of 8% and 2%, respectively. The study is registered at ClinicalTrials.gov (NCT05236699).

Upon doxycycline withdrawal at 8 weeks of age, mice developed progressive cerebellar ataxia by 26 weeks and succumbed by 30 weeks...Prophylactic administration of the CSF1R inhibitor BLZ945 exacerbated motor deficits and demyelination, significantly increasing this microglial population. Similarly, MSR1+ and CD68+ microglia/macrophages were observed in early pontocerebellar lesions of six human MSA-C autopsy cases. These findings suggest that this pro-inflammatory microglia subset plays a central role in disease progression and may represent a promising therapeutic target for modifying the course of MSA-C and related synucleinopathies.

P=N/A, N=80, Not yet recruiting, Blueprint Medicines Corporation

P1/2, N=155, Active, not recruiting, Fujian Haixi Pharmaceuticals Co., Ltd. | Recruiting --> Active, not recruiting

Functional validation was conducted using a ccRCC xenograft mouse model treated with the CSF1R inhibitor Sotuletinib...Importantly, CellChat-based predictions represent potential, rather than definitive, ligand-receptor interactions, and thus require further mechanistic validation. Targeting CSF1R may offer a promising strategy to modulate the immune landscape and improve therapeutic outcomes in ccRCC.

Microglia inhibition or depletion by treating organotypic cultures with minocycline or PLX3397 resulted in reduced levels of all the evaluated cytokines in the medium, confirming the role of microglia in the inflammatory microenvironment of glioblastoma. These findings provide valuable insights into how microglia interact with tumors and healthy cells in the tumor microenvironment, driving neuroinflammation and tumor cell dedifferentiation. This understanding could pave the way for the development of innovative therapies for glioblastoma.

P1, N=20, Completed, Abbisko Therapeutics Co, Ltd | Active, not recruiting --> Completed

Increasing evidence suggests that a subset of CCA patients can benefit from multiple tyrosine kinase inhibitors (mTKIs) such as surufatinib...Furthermore, cancer-associated fibroblasts (CAFs) were identified as the major source of IGF1 in CCA microenvironment, essential for IGF1R-driven tumor progression.In summary, the PTPN9-IGF1R axis plays a pivotal role in modulating mTKI sensitivity and tumor progression in CCA. This axis serves as a promising biomarker for identifying potential mTKI beneficiaries and represents a potential therapeutic target to enhance mTKI efficacy and overcome resistance.

This system, MRC1-targeting peptide-M@BLZ945 (PMMB), integrates a colony-stimulating factor 1 receptor (CSF-1R) inhibitor and a STING agonist within a macrophage-mimetic nanostructure, enabling sequential, controlled reprogramming of TAMs...These findings establish spatiotemporal macrophage circuit engineering via STING phase separation as a cross-scale strategy to override PDAC's immune barriers and drive next-generation macrophage-targeted immunotherapy. This study paves the way for rationally designed, precision macrophage modulation strategies in solid tumors.