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SML2632

Sigma-Aldrich

Autophinib

≥98% (HPLC)

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Synonym(s):
6-Chloro-N-(5-methyl-1H-pyrazol-3-yl)-2-(4-nitrophenoxy)-4-pyrimidinamine, 6-Chloro-N-(5-methyl-1H-pyrazol-3-yl)-2-(4-nitrophenoxy)pyrimidin-4-amine
Empirical Formula (Hill Notation):
C14H11ClN6O3
CAS Number:
Molecular Weight:
346.73
MDL number:

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

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This Item
SML1276B1186SML2567
vibrant-m

SML2632

Autophinib

vibrant-m

SML1276

BAZ2-ICR

vibrant-m

B1186

Binucleine 2

vibrant-m

SML2567

LY2784544

form

powder

form

powder

form

solid

form

powder

color

white to beige

color

white to beige

color

-

color

white to beige

solubility

DMSO: 2 mg/mL, clear

solubility

DMSO: 10 mg/mL, clear

solubility

DMSO: soluble >5 mg/mL, H2O: insoluble

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

2-8°C

Biochem/physiol Actions

Autophinib is an ATP-competitive, potent and selective PI3K type 3 lipid kinase vacuolar protein sorting 34 inhibitor (VPS34 IC50/[ATP] = 19 nM/10 μM & 51 nM/100 μM) that shows significant inhibition against only 45 kinases among a panel of >460 with little or no potency toward mTOR, TBK1 and 12 other phosphatidylinositol kinases (=22% inhibition at 1 μM). Autophinib effectively prevents autophagy induction in MCF7 cells upon amino acid starvation or rapamycin treatment (IC50 = 40 nM and 19 nM, respectively) with similar potency as SAR405 (IC50 = 53 nM and 20 nM, respectively) and VPS34-IN1 (IC50 = 13 nM and 15 nM, respectively). Autophinib enhances MCF7 cell death under starvation condition (EC50 = 264 nM and 234 nM by cytotoxiciy and apoptosis detection, respectively) by preventing autophagy-dependent cell survival.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Lucas Robke et al.
Angewandte Chemie (International ed. in English), 56(28), 8153-8157 (2017-05-26)
Autophagy is a critical regulator of cellular homeostasis and metabolism. Interference with this process is considered a new approach for the treatment of disease, in particular cancer and neurological disorders. Therefore, novel small-molecule autophagy modulators are in high demand. We
Klara Hanelova et al.
Cell communication and signaling : CCS, 21(1), 120-120 (2023-05-25)
Extracellular vesicles (EVs) are important mediators of intercellular communication in the tumour microenvironment. Many studies suggest that cancer cells release higher amounts of EVs exposing phosphatidylserine (PS) at the surface. There are lots of interconnections between EVs biogenesis and autophagy
André Richters et al.
ACS chemical biology, 10(1), 289-298 (2014-12-30)
The cytosolic Ser/Thr kinase TBK1 was discovered to be an essential element in the mediation of signals that lead to tumor migration and progression. These findings meet the need for the identification of novel tool compounds and potential therapeutics to

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