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Results for "

intestinal epithelial damage

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Apoptosis (1) Biochemical Assay Reagents (1) CRFR (2) Environmental Pollutants (1) Heme Oxygenase (HO) (1) Keap1-Nrf2 (1) NO Synthase (1) p38 MAPK (1) Wnt (1) β-catenin (1)
By Research Areas:	Cancer (1) Inflammation/Immunology (3) Metabolic Disease (1) Neurological Disease (2)

Inhibitors & Agonists

Biochemical Assay Reagents

Peptides

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-Y1325I

Sodium acetate trihydrate, 99.5%	Environmental Pollutants Biochemical Assay Reagents Apoptosis NO Synthase p38 MAPK Heme Oxygenase (HO) Keap1-Nrf2 Wnt β-catenin	Metabolic Disease Inflammation/Immunology Cancer
Sodium acetate trihydrate, 99.5% is a short-chain fatty acid salt with multiple biological activities. Sodium acetate trihydrate, 99.5% serves as a direct precursor of acetyl-CoA, and it extensively affects gene expression by promoting histone acetylation. Sodium acetate trihydrate, 99.5% can activate the p38 MAPK pathway to induce cancer cell apoptosis. Sodium acetate trihydrate, 99.5% can activate the Wnt/β-catenin signaling pathway to stimulate the proliferation and migration of cecal epithelial cells, thereby improving intestinal health. Sodium acetate trihydrate, 99.5% alleviates lead accumulation and oxidative damage by upregulating the testosterone-dependent eNOS/NO/cGMP signaling pathway, as well as activating the Nrf2/HO-1 pathway and its downstream antioxidant enzymes .

HY-P1108A

Astressin 2B TFA 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B TFA is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B TFA blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B TFA reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B TFA also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B TFA mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B TFA is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

HY-P1108

Astressin 2B 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

Cat. No.	Product Name	Type

HY-Y1325I

Sodium acetate trihydrate, 99.5%	Biochemical Assay Reagents
Sodium acetate trihydrate, 99.5% is a short-chain fatty acid salt with multiple biological activities. Sodium acetate trihydrate, 99.5% serves as a direct precursor of acetyl-CoA, and it extensively affects gene expression by promoting histone acetylation. Sodium acetate trihydrate, 99.5% can activate the p38 MAPK pathway to induce cancer cell apoptosis. Sodium acetate trihydrate, 99.5% can activate the Wnt/β-catenin signaling pathway to stimulate the proliferation and migration of cecal epithelial cells, thereby improving intestinal health. Sodium acetate trihydrate, 99.5% alleviates lead accumulation and oxidative damage by upregulating the testosterone-dependent eNOS/NO/cGMP signaling pathway, as well as activating the Nrf2/HO-1 pathway and its downstream antioxidant enzymes .

Sodium acetate trihydrate, 99.5%

Biochemical Assay Reagents

Sodium acetate trihydrate, 99.5% is a short-chain fatty acid salt with multiple biological activities. Sodium acetate trihydrate, 99.5% serves as a direct precursor of acetyl-CoA, and it extensively affects gene expression by promoting histone acetylation. Sodium acetate trihydrate, 99.5% can activate the p38 MAPK pathway to induce cancer cell apoptosis. Sodium acetate trihydrate, 99.5% can activate the Wnt/β-catenin signaling pathway to stimulate the proliferation and migration of cecal epithelial cells, thereby improving intestinal health. Sodium acetate trihydrate, 99.5% alleviates lead accumulation and oxidative damage by upregulating the testosterone-dependent eNOS/NO/cGMP signaling pathway, as well as activating the Nrf2/HO-1 pathway and its downstream antioxidant enzymes .

Cat. No.	Product Name	Target	Research Area

HY-P1108A

Astressin 2B TFA 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B TFA is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B TFA blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B TFA reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B TFA also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B TFA mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B TFA is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

HY-P1108

Astressin 2B 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

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BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.

BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

MedchemExpress Validation 03

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred

MedchemExpress Validation 04

MedchemExpress Validation

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