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Sotuletinib

Sotuletinib (BLZ945) is a potent, selective, orally active and brain-penetrant CSF-1R (c-Fms) inhibitor with an IC50 of 1 nM, showing more than 1,000-fold selectivity against its closest receptor tyrosine kinase homologs. Sotuletinib can be used for microglia depletion, and for tumor and CNS-related disease research[1][2][3][4].

Product Specifications

CAS Number

[953769-46-5]

Product Name Alternative

BLZ945

UNSPSC

12352005

Hazard Statement

H302, H315, H319, H335

Target

C-Fms

Type

Reference compound

Related Pathways

Protein Tyrosine Kinase/RTK

Applications

Cancer-Kinase/protease

Field of Research

Cancer; Infection; Neurological Disease

Assay Protocol

https://www.medchemexpress.com/BLZ945.html

Purity

99.97

Solubility

DMSO : 83.33 mg/mL (ultrasonic)

Smiles

O=C(C1=NC=CC(OC2=CC=C3N=C(N[C@H]4[C@H](O)CCCC4)SC3=C2)=C1)NC

Molecular Formula

C20H22N4O3S

Molecular Weight

398.48

Precautions

H302, H315, H319, H335

References & Citations

[1]Pyonteck SM, et al. CSF-1R inhibition alters macrophage polarization and blocks glioma progression. Nat Med. 2013 Oct;19 (10) :1264-72.|[2]Strachan DC, et al. CSF1R inhibition delays cervical and mammary tumor growth in murine models by attenuating the turnover of tumor-associated macrophages and enhancing infiltration by CD8+ T cells. Oncoimmunology. 2013 Dec 1;2 (12) :e26968.|[3]Chen Y, et al. Spatiotemporally selective astrocytic ATP dynamics encode injury information sensed by microglia following brain injury in mice. Nat Neurosci. 2024 Aug;27 (8) :1522-1533.|[4]Frosch M, et al. Microglia-neuron crosstalk through Hex-GM2-MGL2 maintains brain homeostasis. Nature. 2025 Oct;646 (8086) :913-924. |[5]Beckmann N, et al. Brain region-specific enhancement of remyelination and prevention of demyelination by the CSF1R kinase inhibitor BLZ945. Acta Neuropathol Commun. 2018 Feb 15;6 (1) :9.

Shipping Conditions

Room Temperature

Storage Conditions

-20°C, 3 years; 4°C, 2 years (Powder)

Scientific Category

Reference compound1

Clinical Information

Phase 2

Citation 01

Acta Biomater. 2024 Jan 15:174:372-385.|Acta Neuropathol. 2025 May 9;149 (1) :47.|Adv Healthc Mater. 2024 May 28:e2401719.|Adv Sci (Weinh) . 2024 Dec;11 (45) :e2404756.|Anti-Cancer Drug. 2022 Dec.|Bioact Mater. 2022 Mar 11:16:107-119.|bioRxiv. 2024 July 16.|bioRxiv. 2025 Jun 15.|bioRxiv. 2025 May 1:2024.03.05.583602.|bioRxiv. 2025 Oct 13.|Blood. 2019 Nov 28;134 (22) :1929-1940.|Cancer Immunol Res. 2021 Jun;9 (6) :665-681.|Cancer Res Commun. 2024 Oct 1;4 (10) :2638-2652.|Cell Chem Biol. 2022 Jul 21;29 (7) :1113-1125.e6.|Cell Death Dis. 2025 Oct 7;16 (1) :716.|Cell Signal. 2024 Dec 9:111550.|Clin Cancer Res. 2018 Mar 1;24 (5) :1176-1189.|eNeuro. 2021 Mar 22;8 (2) :ENEURO.0318-20.2021.|J Exp Med. 2016 Dec 12;213 (13) :2989-3005.|J Exp Med. 2020 Nov 2;217 (11) :e20191820.|J Exp Med. 2023 Mar 6;220 (3) :e20220857.|J Neuroinflammation. 2024 Oct 3;21 (1) :248.|J Nucl Med. 2025 Feb 3;66 (2) :302-308.|JCI Insight. 2025 Jan 9;10 (1) :e178146.|Mol Ther. 2025 Nov 12.|Nat Biomed Eng. 2018 Aug;2 (8) :578-588.|Nat Neurosci. 2024 Aug;27 (8) :1522-1533.|Neuro Oncol. 2024 Sep 10:noae184.|Proc Natl Acad Sci U S A. 2022 Oct 25;119 (43) :e2207280119.|Res Sq. 2024 Nov 19.|Research Square Preprint. 2024 Dec 03.|Sci Adv. 2023 May 12;9 (19) :eade3559.|Sci Rep. 2022 Nov 2;12 (1) :18521.|Nature. 2025 Oct;646 (8086) :913-924.|SSRN. 2025 Sep 25.

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