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Overview
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Background
Colony stimulating factor-1 (CSF1) is a key cytokine involved in recruitment and activation of tissue macrophages, exerting these effects through binding to a high-affinity receptor tyrosine kinase, the cFMS/CSF1 receptor. Pexidartinib (PLX3397) is a CSF-1R inhibitor that can cross the blood–brain barrier.
In vitro: PLX3397 strongly dampened the systemic and local accumulation of macrophages driven by B16F10 melanomas, without affecting Gr-1+ myeloid derived suppressor cells [1].
In vivo: Wild-type C57 mice were orthotopically injected with GL261 cells and fed with PLX3397 compound. After 2 wks, tumors in the control group showed extensive microglia infiltration. In animals fed PLX3397, however, there was a substantial reduction in the number of Iba1- positive cells at the tumor [2].
Clinical trial: In a phase Ib trial, patients with advanced solid tumors are treated with weekly paclitaxel and escalating doses of oral PLX3397 to establish a RP2D of PLX3397. This study will support further development of the PLX3397-paclitaxel combination in the I-SPY-2 neoadjuvant breast cancer trial.[1] Sluijter M, van der Sluis TC, van der Velden PA, Versluis M, West BL, van der Burg SH, van Hall T. Inhibition of CSF-1R supports T-cell mediated melanoma therapy. PLoS One. 2014 Aug 11;9(8):e104230.
[2] Coniglio SJ, Eugenin E, Dobrenis K, Stanley ER, West BL, Symons MH, Segall JE. Microglial stimulation of glioblastoma invasion involves epidermal growth factor receptor (EGFR) and colony stimulating factor 1 receptor (CSF-1R) signaling. Mol Med. 2012 May 9;18:519-27.
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