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Methyl cyclohexanecarboxylate

" in MedChemExpress (MCE) Product Catalog:

By Targets:	CRFR (2) Endogenous Metabolite (1) Fungal (1) Reference Standards (1)
By Research Areas:	Infection (1) Inflammation/Immunology (2) Metabolic Disease (1) Neurological Disease (2)

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Cat. No.	Product Name	Target	Research Areas	Chemical Structure

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 .

HY-W007704

**Methyl cyclohexanecarboxylate**	Fungal	Infection
Methyl cyclohexanecarboxylate is a compound related to 2-cyclohexenylcarbonyl CoA. Methyl cyclohexanecarboxylate is produced during the incubation of 2-cyclohexenylcarbonyl CoA with cell-free extracts of Streptomyces collinus .

HY-W007704R

Methyl cyclohexanecarboxylate (Standard)	Reference Standards Endogenous Metabolite	Metabolic Disease
Methyl cyclohexanecarboxylate (Standard) is the analytical standard of Methyl cyclohexanecarboxylate. This product is intended for research and analytical applications. Methyl cyclohexanecarboxylate is an endogenous metabolite.

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 .

**Methyl cyclohexanecarboxylate**	Structural Classification Natural Products Classification of Application Fields Metabolic Disease Endogenous metabolite Disease Research Fields Source Classification	Fungal
Methyl cyclohexanecarboxylate is a compound related to 2-cyclohexenylcarbonyl CoA. Methyl cyclohexanecarboxylate is produced during the incubation of 2-cyclohexenylcarbonyl CoA with cell-free extracts of Streptomyces collinus .

Methyl cyclohexanecarboxylate (Standard)	Structural Classification Natural Products Endogenous metabolite Source Classification	Reference Standards Endogenous Metabolite
Methyl cyclohexanecarboxylate (Standard) is the analytical standard of Methyl cyclohexanecarboxylate. This product is intended for research and analytical applications. Methyl cyclohexanecarboxylate is an endogenous metabolite.

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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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Methyl cyclohexanecarboxylate

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