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4-Bromo-3-hydroxybenzoic acid Sale

(Synonyms: 4-溴-3-羟基苯甲酸) 目录号 : GC39473

4-Bromo-3-hydroxybenzoic acid 是一种 Brocresine 的代谢产物,也是一种组氨酸脱羧酶 (HDC) 抑制剂,对大鼠胎儿和大鼠胃 HDC 的 IC50 均为 1 mM。4-Bromo-3-hydroxybenzoic acid 还可以在体外抑制猪肾脏和大鼠胃粘膜中的芳香族 L-氨基酸脱羧酶 (aromatic-L-amino acid decarboxylase),两种酶的 IC50 均为 1 mM。

4-Bromo-3-hydroxybenzoic acid Chemical Structure

Cas No.:14348-38-0

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100mg
¥495.00
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产品描述

4-Bromo-3-hydroxybenzoic acid is a metabolite of Brocresine and a histidine decarboxylase (HDC) inhibitor with IC50s of 1 mM for both rat fetal and rat gastric HDC. 4-Bromo-3-hydroxybenzoic acid also inhibits aromatic-L-amino acid decarboxylase from hog kidney and rat gastric mucosa in vitro with IC50s of 1 mM for both enzymes[1][2].

[1]. Ellenbogen L, et al. Studies on the inhibition of histidine decarboxylase, aromatic-L-amino acid decarboxylase and acid secretion by brocresine and its metabolites. Biochem Pharmacol. 1973 Apr 15;22(8):939-47. [2]. Qian S, et al. Inhibiting Histamine Signaling Ameliorates Vertigo Induced by Sleep Deprivation. J Mol Neurosci. 2019 Mar;67(3):411-417.

Chemical Properties

Cas No. 14348-38-0 SDF
别名 4-溴-3-羟基苯甲酸
Canonical SMILES BrC1=C(O)C=C(C(O)=O)C=C1
分子式 C7H5BrO3 分子量 217.02
溶解度 DMSO : 100 mg/mL (460.79 mM; Need ultrasonic) 储存条件 Store at -20°C
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1 mM 4.6079 mL 23.0394 mL 46.0787 mL
5 mM 0.9216 mL 4.6079 mL 9.2157 mL
10 mM 0.4608 mL 2.3039 mL 4.6079 mL
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Research Update

Biomarkers of PEGylated Liposomal Doxorubicin-Induced Hypersensitivity Reaction in Breast Cancer Patients Based on Metabolomics

Front Pharmacol 2022 Apr 21;13:827446.PMID:35529437DOI:10.3389/fphar.2022.827446.

This study aimed to analyze and discuss the biomarkers of PEGylated liposomal doxorubicin (PLD) injection-induced hypersensitivity reactions (HSRs) in advanced breast cancer patients. Fourteen patients from Sun Yat-sen Memorial Hospital were included in the study between April 15th, 2020 and April 14th, 2021. Patient plasma was collected 30 min before PLD injection. HSRs were found to occur in a total of 9 patients (64.3%). No association was found between HSRs and various patient characteristics such as age, body surface area, anthracycline treatment history, IgE, and complement 3 and 4 (p > 0.05). Non-targeted metabolomics analysis of patient plasma was performed, and several metabolites showed significant association with HSRs. In particular, l-histidine (fold change = 91.5, p = 0.01) showed significantly higher levels in the immediate HSR group, while myristicin (fold change = 0.218, p = 0.003), urocanic acid (fold change = 0.193, p = 0.007), and d-aldose (fold change = 0.343, p = 0.003) showed significantly lower levels in the same group. In vivo experiments showed that exogenous histidine aggravated HSRs and increased IgE plasma levels in rats following the injection of PLD. Histidine can be decarboxylated to histamine by histidine decarboxylase. Histidine decarboxylase inhibitor 4-Bromo-3-hydroxybenzoic acid improved symptoms and IgE levels in vivo. These findings suggested that l-histidine can be a potential biomarker for PLD-induced HSR. Moreover, an antihistamine drug, histidine decarboxylase inhibitor, or dietary histidine management could be used as potential preventive measures. Furthermore, metabolomics research could serve as a powerful method to explore biomarkers or uncover mechanisms of drug side effects.

Inhibiting Histamine Signaling Ameliorates Vertigo Induced by Sleep Deprivation

J Mol Neurosci 2019 Mar;67(3):411-417.PMID:30644035DOI:10.1007/s12031-018-1244-6.

Although histamine inhibitors have been used in the motility-associated vertigo, the link between histamine and sleep deprivation (SD)-induced vertigo has not been clearly demonstrated. The histamine plasma levels were assayed in the SD volunteers before SD and 24 h after SD. Pinnacle's automated sleep deprivation system was used to establish the female C57BL/6 mice SD model. Histidine decarboxylase inhibitor 4-Bromo-3-hydroxybenzoic acid (BHOA), and antihistamine diphenhydramine (DPHM) were injected intraperitoneally to test their effects on SD-induced vertigo. Rotarod tests and vestibular scores 24 and 48 h post SD were utilized to assay the vestibular function. Western blot was used to determine the expression of histidine decarboxylase (HDC) in the vestibular, and PowerChrom was utilized to quantify the concentrations of cerebrospinal fluid (CSF) histamine. SD increased plasma concentration of histamine in humans. Upregulated HDC in the vestibular and increased CSF concentration of histamine can be detected in the SD mice, indicating vestibular dysfunction which can be ameliorated by both BHOA and DPHM. Histamine signaling inhibition may ameliorate SD-induced vertigo, and histamine can be considered as a potential treatment target.