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2,4-Dihydroxybenzoic acid Sale

(Synonyms: 2,4-二羟基苯甲酸) 目录号 : GC33626

2,4-Dihydroxybenzoic acid (β-resorcylic acid, p-Hydroxysalicylic acid) is a degradation product of cyanidin glycosides from tart cherries in cell cultures and a metabolite found in human plasma after cranberry juice consumption.

2,4-Dihydroxybenzoic acid Chemical Structure

Cas No.:89-86-1

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产品描述

2,4-Dihydroxybenzoic acid (β-resorcylic acid, p-Hydroxysalicylic acid) is a degradation product of cyanidin glycosides from tart cherries in cell cultures and a metabolite found in human plasma after cranberry juice consumption.

Chemical Properties

Cas No. 89-86-1 SDF
别名 2,4-二羟基苯甲酸
Canonical SMILES O=C(O)C1=CC=C(O)C=C1O
分子式 C7H6O4 分子量 154.12
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mM 6.4885 mL 32.4423 mL 64.8845 mL
5 mM 1.2977 mL 6.4885 mL 12.9769 mL
10 mM 0.6488 mL 3.2442 mL 6.4885 mL
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Research Update

Hypouricemic effect of 2,4-Dihydroxybenzoic acid methyl ester in hyperuricemic mice through inhibiting XOD and down-regulating URAT1

Biomed Pharmacother 2022 Sep;153:113303.PMID:35750011DOI:10.1016/j.biopha.2022.113303.

In this paper, we reported the hypouricemic effect of 2,4-Dihydroxybenzoic acid methyl ester (DAE), a component of Ganoderma applanatum, in hyperuricemic mice through inhibiting XOD and down-regulating URAT1. Computationally, DAE showed a high similarity to allopurinol and depicted a high affinity in docking to XOD. In vitro, DAE exhibited an inhibitory effect against XOD. Importantly, DAE demonstrated a remarkable hypouricemic effect, decreasing serum uric acids (SUAs) of hyperuricemic mice (407 ± 31 μmol/L) to 195 ± 23, 145 ± 33 and 134 ± 16 μmol/L (P < 0.01) at the doses of 20, 40, and 80 mg/kg with a dose-dependent manner and showing efficacies at 54-68 %, which were close to the efficacies of allopurinol (61 %) and benzbromarone (57 %). DAE depicted higher and negatively dose-independent urinary uric acids in comparison with that of the hyperuricemic control, implying DAE exerted an uricosuric effect and also a reduction effect on uric acid production. Unlike toxic allopurinol and benzbromarone, no general toxicity on body weights and no negative influence on liver, kidney, spleen and thymus were observed for DAE. Mechanistically, DAE inhibited XOD activities in vivo. Moreover, DAE up-regulated OAT1 and down-regulated GLUT9, URAT1 and CNT2. Overall, DAE may present a hypouricemic effect through inhibiting XOD and up-regulating OAT1 and down-regulating GLUT9, URAT1 and CNT2. This work provided novel insights into the hypouricemic effect of DAE and G. applanatum.

Electrostatic properties of the pyrimethamine-2,4-dihydroxybenzoic acid cocrystal in methanol studied using transferred electron-density parameters

Acta Crystallogr C Struct Chem 2018 Jan 1;74(Pt 1):100-107.PMID:29303503DOI:10.1107/S2053229617017788.

The crystal structure of the cocrystal salt form of the antimalarial drug pyrimethamine with 2,4-Dihydroxybenzoic acid in methanol [systematic name: 2,4-diamino-5-(4-chlorophenyl)-6-ethylpyrimidin-1-ium 2,4-dihydroxybenzoate methanol monosolvate, C12H14ClN4+·C7H5O4-·CH3OH] has been studied using X-ray diffraction data collected at room temperature. The crystal structure was refined using the classical Independent Atom Model (IAM) and the Multipolar Atom Model by transferring electron-density parameters from the ELMAM2 database. The Cl atom was refined anharmonically. The results of both refinement methods have been compared. The intermolecular interactions have been characterized on the basis of Hirshfeld surface analysis and topological analysis using Bader's theory of Atoms in Molecules. The results show that the molecular assembly is built primarily on the basis of charge transfer between 2,4-Dihydroxybenzoic acid and pyrimethamine, which results in strong intermolecular hydrogen bonds. This fact is further validated by the calculation of the electrostatic potential based on transferred electron-density parameters.

Potential of 2,4-Dihydroxybenzoic acid as an Oviposition Stimulant for Mass-Reared Ladybird Beetles

J Insect Sci 2019 Mar 1;19(2):9.PMID:30822780DOI:10.1093/jisesa/iez012.

The discovery of inexpensive, readily available bioflavonoids, and their degradation products that boost the reproductive potential of mass-reared predators is the overarching goal of this research. We tested the hypothesis that 2,4-Dihydroxybenzoic acid (DHBA), an inexpensive degradation product of morin (a flavonol bioflavonoid), stimulates oviposition by the ladybird beetle Coleomegilla maculata (DeGeer). We also tested the hypothesis that C. maculata females must touch or taste DHBA to stimulate oviposition. We setup bioassays in communal cages (housing 10 females) and solitary cages (housing 1 female). In communal cages, nearly all egg clutches were found in or near the chemical dish with DHBA only. Provisioning cages with a tissue substrate reduced oviposition in the chemical dish. Regardless of oviposition site, egg number per clutch did not increase in communal cages or solitary cages with DHBA only. Affixing DHBA to the base of the chemical dish, then covering it with a nylon screen, reduced oviposition. This study suggests that females must touch or taste DHBA to stimulate oviposition. The physiological mechanism involved in oviposition stimulation requires further study. DHBA could potentially serve as a weak oviposition stimulant for predatory ladybird beetles in some mass-rearing systems.

Treatment with 2,4-Dihydroxybenzoic acid Prevents FSGS Progression and Renal Fibrosis in Podocyte-Specific Coq6 Knockout Mice

J Am Soc Nephrol 2019 Mar;30(3):393-405.PMID:30737270DOI:10.1681/ASN.2018060625.

Background: Although studies have identified >55 genes as causing steroid-resistant nephrotic syndrome (SRNS) and localized its pathogenesis to glomerular podocytes, the disease mechanisms of SRNS remain largely enigmatic. We recently reported that individuals with mutations in COQ6, a coenzyme Q (also called CoQ10, CoQ, or ubiquinone) biosynthesis pathway enzyme, develop SRNS with sensorineural deafness, and demonstrated the beneficial effect of CoQ for maintenace of kidney function. Methods: To study COQ6 function in podocytes, we generated a podocyte-specific Coq6 knockout mouse (Coq6podKO ) model and a transient siRNA-based COQ6 knockdown in a human podocyte cell line. Mice were monitored for development of proteinuria and assessed for development of glomerular sclerosis. Using a podocyte migration assay, we compared motility in COQ6 knockdown podocytes and control podocytes. We also randomly assigned 5-month-old Coq6podKO mice and controls to receive no treatment or 2,4-Dihydroxybenzoic acid (2,4-diHB), an analog of a CoQ precursor molecule that is classified as a food additive by health authorities in Europe and the United States. Results: Abrogation of Coq6 in mouse podocytes caused FSGS and proteinuria (>46-fold increases in albuminuria). In vitro studies revealed an impaired podocyte migration rate in COQ6 knockdown human podocytes. Treating Coq6podKO mice or cells with 2,4-diHB prevented renal dysfunction and reversed podocyte migration rate impairment. Survival of Coq6podKO mice given 2,4diHB was comparable to that of control mice and significantly higher than that of untreated Coq6podKO mice, half of which died by 10 months of age. Conclusions: These findings reveal a potential novel treatment strategy for those cases of human nephrotic syndrome that are caused by a primary dysfunction in the CoQ10 biosynthesis pathway.

ADCK4 Deficiency Destabilizes the Coenzyme Q Complex, Which Is Rescued by 2,4-Dihydroxybenzoic acid Treatment

J Am Soc Nephrol 2020 Jun;31(6):1191-1211.PMID:32381600DOI:10.1681/ASN.2019070756.

Background: Mutations in ADCK4 (aarF domain containing kinase 4) generally manifest as steroid-resistant nephrotic syndrome and induce coenzyme Q10 (CoQ10) deficiency. However, the molecular mechanisms underlying steroid-resistant nephrotic syndrome resulting from ADCK4 mutations are not well understood, largely because the function of ADCK4 remains unknown. Methods: To elucidate the ADCK4's function in podocytes, we generated a podocyte-specific, Adck4-knockout mouse model and a human podocyte cell line featuring knockout of ADCK4. These knockout mice and podocytes were then treated with 2,4-Dihydroxybenzoic acid (2,4-diHB), a CoQ10 precursor analogue, or with a vehicle only. We also performed proteomic mass spectrometry analysis to further elucidate ADCK4's function. Results: Absence of Adck4 in mouse podocytes caused FSGS and albuminuria, recapitulating features of nephrotic syndrome caused by ADCK4 mutations. In vitro studies revealed that ADCK4-knockout podocytes had significantly reduced CoQ10 concentration, respiratory chain activity, and mitochondrial potential, and subsequently displayed an increase in the number of dysmorphic mitochondria. However, treatment of 3-month-old knockout mice or ADCK4-knockout cells with 2,4-diHB prevented the development of renal dysfunction and reversed mitochondrial dysfunction in podocytes. Moreover, ADCK4 interacted with mitochondrial proteins such as COQ5, as well as cytoplasmic proteins such as myosin and heat shock proteins. Thus, ADCK4 knockout decreased the COQ complex level, but overexpression of ADCK4 in ADCK4-knockout podocytes transfected with wild-type ADCK4 rescued the COQ5 level. Conclusions: Our study shows that ADCK4 is required for CoQ10 biosynthesis and mitochondrial function in podocytes, and suggests that ADCK4 in podocytes stabilizes proteins in complex Q in podocytes. Our study also suggests a potential treatment strategy for nephrotic syndrome resulting from ADCK4 mutations.