Indole-4-carboxaldehyde


CAS No. : 1074-86-8

1074-86-8
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Cat. No. : HY-W001288
M.Wt: 145.16
Formula: C9H7NO
Purity: >98 %
Solubility: DMSO : 50 mg/mL (ultrasonic)
Introduction of 1074-86-8 :

Indole-4-carboxaldehyde is an ergot alkaloid precursor that regulates glycosylation and inflammation. Indole-4-carboxaldehyde upregulates Glo-1, inhibits MGO-induced NF-κB activation, and suppresses MGO-induced expression of TNF-α and IFN-γ. Indole-4-carboxaldehyde inhibits MGO-induced formation of advanced glycation end products (AGE) and expression of their receptor (RAGE). Indole-4-carboxaldehyde is a core metabolite produced in the pedicels of Summer Black grapes after exogenous gibberellin treatment, and it directly promotes fruit enlargement and fruit set of Summer Black grapes. Indole-4-carboxaldehyde can be used in studies related to hepatic steatosis and plant growth regulation[1][2][3]. In Vitro:Indole-4-carboxaldehyde (ST-14C) (50-200 µM; 24 h) induces the proliferation of HepG2 cells at concentrations of 50 µM and 100 µM[1].
Indole-4-carboxaldehyde (25-200 µM; 6-24 h) induces a dose-dependent increase in Glo-1 mRNA and protein expression, and enhances the fluorescence intensity of Glo-1 in HepG2 cells[1].
Indole-4-carboxaldehyde reacts with 4-substituted thiosemicarbazides in refluxing ethanol to form thioformamide derivatives[2].
Indole-4-carboxaldehyde shows significant upregulation and directly promotes fruit enlargement and fruit set of the pedicels of Summer Black grapes treated twice with exogenous gibberellin[3].
Indole-4-carboxaldehyde (100 µM; 2 h pre-incubation prior to 4 h MGO exposure) attenuates the expression of TNF-α, IFN-γ and RAGE mRNA in MGO-induced HepG2 cells, and inhibits the nuclear translocation of NF-κB p65[1].
Indole-4-carboxaldehyde (100 µM; 2 h pre-incubation prior to 24 h MGO exposure) reduces methylglyoxal-induced secretion of TNF-α and IFN-γ in HepG2 cells and attenuates the formation of AGE[1].
Indole-4-carboxaldehyde (100 µM; 2 h pre-incubation prior to 4-24 h MGO exposure) fails to attenuate MGO-induced IFN-γ mRNA expression and AGE formation in Glo-1-knockdown HepG2 cells, indicating that these effects are mediated by Glo-1[1].

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