Homocarbonyltopsentin

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Company Name: Shanghai YuanYe Biotechnology Co., Ltd.  
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Tel: 15317229551
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Homocarbonyltopsentin manufacturers

Homocarbonyltopsentin Basic information
Product Name:Homocarbonyltopsentin
Synonyms:Homocarbonyltopsentin;PK4C9;Methanone, [2-[(6-hydroxy-1H-indol-3-yl)carbonyl]-1H-imidazol-4-yl]-1H-indol-3-yl- (9CI)
CAS:172286-77-0
MF:C21H14N4O3
MW:370.36
EINECS:
Product Categories:
Mol File:172286-77-0.mol
Homocarbonyltopsentin Structure
Homocarbonyltopsentin Chemical Properties
Melting point >210 °C
Boiling point 801.2±75.0 °C(Predicted)
density 1.539±0.06 g/cm3(Predicted)
storage temp. Store at -20°C
solubility DMSO: 125 mg/mL (337.51 mM)
pka7.50±0.10(Predicted)
form Solid
color White to yellow
InChI1S/C21H14N4O3/c26-11-5-6-13-15(9-23-17(13)7-11)20(28)21-24-10-18(25-21)19(27)14-8-22-16-4-2-1-3-12(14)16/h1-10,22-23,26H,(H,24,25)
InChIKeyDRCVQVIMGSWRLN-UHFFFAOYSA-N
SMILES[nH]1c(nc(c1)C(=O)c4c5c([nH]c4)cccc5)C(=O)c2c3c([nH]c2)cc(cc3)O
Safety Information
WGK Germany WGK 3
Storage Class11 - Combustible Solids
MSDS Information
Homocarbonyltopsentin Usage And Synthesis
UsesHomocarbonyltopsentin (PK4C9) is a small-molecule TSL2-binding compound, binds to pentaloop conformations of TSL2 and promotes a shift to triloop conformations that display enhanced SMN2 exon 7 (E7) splicing with EC50 value of 16 μM[1].
Biological ActivityPK4C9 is a splice modulator of survival of motor neuron gene SMN2 th at increases production of full-length SMN protein. Spinal muscular atrophy (SMA) is a motor neuron disease caused by deficiency in SMN protein resulting from loss of expression of the SMN1 gene. The related SMN2 gene can compensate, but polymorphism in SMN2 often results in altered splicing and exclusion of exon 7, which is required for a full-length SMN transcript. PK4C9 binds to pentaloop conformations of the stem-loop RNA structure TSL2, a cis-regulatory element for E7 inclusion, and promotes a shift to triloop conformations th at display enhanced E7 splicing. In SMA cells, PK4C9 increased E7 inclusion by 40% accompanied by a 1.5-fold increase in SMN protein, a level shown to reverse SMA phenotypes in mice models.
References[1] Garcia-Lopez A, et al. Targeting RNA structure in SMN2 reverses spinal muscular atrophy molecular phenotypes. Nat Commun. 2018 May 23;9(1):2032. DOI:10.1038/s41467-018-04110-1
Homocarbonyltopsentin Preparation Products And Raw materials
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