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SML3673

Sigma-Aldrich

Lin28 inhibitor C1632

≥98% (HPLC)

Sinónimos:

Lin28 1632, Lin28 inhibitor I, Lin28-C1632, Lin28-let-7 antagonist 1, N-Methyl-N-[3-(3-methyl[1,2,4]triazolo[4,3-b]pyridazin-6-yl)phenyl]acetamide

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About This Item

Fórmula empírica (notación de Hill):
C15H15N5O
Número de CAS:
108825-65-6
Peso molecular:
281.31
MDL number:
MFCD01567008
UNSPSC Code:
12352200
NACRES:
NA.28

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

, White to light Brown

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

Biochem/physiol Actions

Compound 1632 (C1632) is a RNA-binding protein Lin28 inhibitor that prevents Lin28-mediated inhibition of let-7 microRNA (miRNA) maturation by blocking Lin28 interaction with let-7 miRNA precursor (IC50 = 8 μM by ELISA using truncated pre-let-7a-2). C1632 specifically upregulates Huh7 cellular let-7a/g/f miRNA, but not RNU44 snoRNA (60 μM for 48h), inhibits the stemness and induces differentiation of mouse embryonic stem cells (mESCs, 20 μM for 48h), as well as inhibits the proliferation and stem-like properties of human cancer stem cells (CSCs) in 22Rv1 and Huh7 cultures (IC50 20-42 μM).

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Martina Roos et al.
ACS chemical biology, 11(10), 2773-2781 (2016-10-22)
New discoveries in RNA biology underscore a need for chemical tools to clarify their roles in pathophysiological mechanisms. In certain cancers, synthesis of the let-7 microRNA tumor suppressor is blocked by an RNA binding protein (RBP) Lin28, which docks onto
Pharmacological inhibition of Lin28 promotes ketogenesis and restores lipid homeostasis in models of non-alcoholic fatty liver disease
Nature Communications, 13(1), 7940-7940 (2022)
Jing-Yi Chen et al.
Journal of cellular and molecular medicine, 26(2), 422-435 (2021-12-17)
Chemoresistance and migration represent major obstacles in the therapy of non-small-cell lung cancer (NSCLC), which accounts for approximately 85% of lung cancer patients in clinic. In the present study, we report that the compound C1632 is preferentially distributed in the

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