CSF1R (Colony stimulating factor 1 receptor)

Furthermore, we examine emerging therapeutic strategies targeting glial-specific pathways, including NF-κB, JAK/STAT, CSF1R, and TREM2 signaling, as well as remyelinating agents and stem cell-based interventions. By integrating glial biology with therapeutic innovation, this review positions glial cells not as supporting actors but as central regulators and potential gatekeepers of dementia pathogenesis and treatment.

We also assess challenges in clinical translation, including tumor-type heterogeneity, insufficient biomarkers, and incomplete understanding of spatial immune architecture within bone lesions. Advancing myeloid-targeted interventions may enable more durable control of metastasis and improve outcomes for patients with skeletal involvement.

Also underscored are the existence of commercially available drugs and patented compounds, as well as translational candidates featuring the 2-aminobenzothiazole pharmacophore. The paper emphasises the dual mechanistic targetability of 2-aminobenzothiazole derivatives as valuable lead compounds targeting both kinases and other targets in an innovative manner aimed at future development of targeted anti-cancer therapies.

Our study demonstrates that the OPN/PI3K/AKT/CSF1-CSF1R axis plays a crucial role in CRC metastasis. Blocking the CSF1/CSF1R axis reduces M2-like TAMs infiltration and tumor metastasis, offering a promising strategy for metastatic CRC.

The following ten drugs received FDA approval in 2025 - avutometinib (inhibiting MEK1/2 in serous ovarian carcinomas), defactinib (blocking FAK in low grade serous ovarian carcinomas), delgocitinib (antagonizing the JAK family in hand eczema), mirdametinib (inhibiting MEK1/2 in type I neurofibromatosis), remibrutinib (blocking BTK in chronic spontaneous urticaria), rilzabrutinib (antagonizing BTK in chronic immune thrombocytopenia), sunvozertinib (blocking mutant exon 21 insertion EGFR NSCLC), taletrectinib (inhibiting mutant ROS1 in NSCLC), vimseltinib (blocking CSF1R in tenosynovial giant cell tumors), and zongertinib (antagonizing mutant HER2 in NSCLC). This article summarizes the physicochemical properties of all 94 FDA-approved small molecule protein kinase inhibitors including the molecular weight, number of hydrogen bond donors/acceptors, ligand efficiency, lipophilic efficiency, polar surface area, and solubility. A total of 45 of the 94 FDA-approved drugs have a least one Lipinski rule of five violation.

Furthermore, there is an absence of severe toxicities that have arisen with other agents in the TGCT treatment space, specifically liver failure. Vimseltinib is a favorable option for patients with TGCTs and further efforts to determine its place in the sequence of overall management are needed.

We outline current and emerging myeloid-reprogramming strategies-including PI3Kγ and CSF1-CSF1R targeting, TREM2 antagonism, COX-2-PGE2 blockade, and adenosine-axis inhibition-and their integration with PD-(L)1 therapy, alongside single-cell/spatial endpoints to quantify on-treatment remodeling. The purpose of this mini-review is to provide a mechanistic and technology-informed framework to reference rational trial design and clinical translation for overcoming checkpoint resistance in CRC.

RNA transcriptome sequencing of the subject's tumor showed overexpression of SLC29A11 (Z-score = 3.3) indicating sensitivity to gemcitabine as well as activation of the biological pathways mTOR, CSF1R, EPHA2, SLC29A1, suggesting possible beneficial treatment with a combination of everolimus, gemcitabine, doxycycline and dasatinib. The subject responded to the novel drug combination, continuing medications for 5 years with some modifications, and remained on everolimus alone for an additional 4 years with a complete response, no serious adverse events, and excellent quality of life. In conclusion, Molecular Guided Therapy with tumor board recommendations resulted in a novel therapeutic approach leading to long term survival which correlated to response in vitro.

Finally, CSF1R inhibition on a KMT2A::MLLT3+ paediatric leukaemia cell line resulted in significant cell death, suggesting that CSF1R could be therapeutically targeted in these patients. Our findings suggest that KMT2A::MLLT3+ infant AML may originate from foetal liver CSF1R+ LMPPs, and that these patients may benefit from anti-CSF1R-CAR-T cell therapy.

WHPB targets CSF-1R to suppress FUT8 via PI3K/AKT signaling, blocking key fibrotic pathways. These findings support WHPB's development as a targeted therapy that suppresses FUT8 for RIF.

P=N/A, N=20, Enrolling by invitation, Mayo Clinic | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027