Isobavachin
(Synonyms: 异补骨脂黄酮) 目录号 : GC39036
Isobavachin 是可从 Psoralea morisiana 中分离得到的一种抗氧化剂，在A环的8号位置有一个prenyl基团，它可以促进神经元的分化和其蛋白异戊烯化的潜在作用。
Cas No.:31524-62-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Isobavachin, an antioxidant isaolated from Psoralea morisiana with a prenyl group at position 8 of ring A, promotes neuronal differentiation and the potential role of its protein prenylation[1][2].
[1]. Wang DY, et al. Promoting effects of isobavachin on neurogenesis of mouse embryonic stem cells were associated with protein prenylation. Acta Pharmacol Sin. 2011 Apr;32(4):425-32. [2]. Antonella Rosa, et al. Antioxidant properties of extracts and compounds from Psoralea morisiana. European Journal of Lipid Science and Technology. 2005.
| Cas No. | 31524-62-6 | SDF | |
| 别名 | 异补骨脂黄酮 | ||
| Canonical SMILES | O=C1C[C@@H](C2=CC=C(O)C=C2)OC3=C(C/C=C(C)\C)C(O)=CC=C13 | ||
| 分子式 | C20H20O4 | 分子量 | 324.37 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.0829 mL | 15.4145 mL | 30.829 mL |
| 5 mM | 0.6166 mL | 3.0829 mL | 6.1658 mL |
| 10 mM | 0.3083 mL | 1.5414 mL | 3.0829 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Investigation on the metabolic characteristics of Isobavachin in Psoralea corylifolia L. (Bu-gu-zhi) and its potential inhibition against human cytochrome P450s and UDP-glucuronosyltransferases
J Pharm Pharmacol 2020 Dec;72(12):1865-1878.PMID:32750744DOI:10.1111/jphp.13337.
Objectives: Isobavachin is a phenolic with anti-osteoporosis activity. This study aimed to explore its metabolic fates in vivo and in vitro, and to investigate the potential drug-drug interactions involving CYPs and UGTs. Methods: Metabolites of Isobavachin in mice were first identified and characterized. Oxidation and glucuronidation study were performed using liver and intestine microsomes. Reaction phenotyping, activity correlation analysis and relative activity factor approaches were employed to identify the main CYPs and UGTs involved in Isobavachin metabolism. Through kinetic modelling, inhibition mechanisms towards CYPs and UGTs were also explored. Key findings: Two glucuronides (G1 - G2) and three oxidated metabolites (M1 - M3) were identified in mice. Additionally, Isobavachin underwent efficient oxidation and glucuronidation by human liver microsomes and HIM with CLint values from 5.53 to 148.79 μl/min per mg. CYP1A2, 2C19 contributed 11.3% and 17.1% to hepatic metabolism of Isobavachin, respectively, with CLint values from 8.75 to 77.33 μl/min per mg. UGT1As displayed CLint values from 10.73 to 202.62 μl/min per mg for glucuronidation. Besides, significant correlation analysis also proved that CYP1A2, 2C19 and UGT1A1, 1A9 were main contributors for the metabolism of Isobavachin. Furthermore, mice may be the appropriate animal model for predicting its metabolism in human. Moreover, Isobavachin exhibited broad inhibition against CYP2B6, 2C9, 2C19, UGT1A1, 1A9, 2B7 with Ki values from 0.05 to 3.05 μm. Conclusions: CYP1A2, 2C19 and UGT1As play an important role in Isobavachin metabolism. Isobavachin demonstrated broad-spectrum inhibition of CYPs and UGTs.
Mechanism of anti-hyperuricemia of Isobavachin based on network pharmacology and molecular docking
Comput Biol Med 2023 Mar;155:106637.PMID:36791549DOI:10.1016/j.compbiomed.2023.106637.
Background: Hyperuricemia is a more popular metabolic disease caused by a disorder of purine metabolism. Our previous study firstly screened out a natural product Isobavachin as anti-hyperuricemia targeted hURAT1 from a Chinese medicine Haitongpi (Cortex Erythrinae). In view of Isobavachin's diverse pharmacological activities, similar to the Tranilast (as another hURAT1 inhibitor), our study focused on its potential targets and molecular mechanisms of Isobavachin anti-hyperuricemia based on network pharmacology and molecular docking. Methods: First of all, the putative target genes of compounds were screen out based on the public databases with different methods, such as SwissTargetPerdiction, PharmMapper and TargetNet,etc. Then the compound-pathways were obtained by the compounds' targets gene from David database for Gene Ontology (GO) function enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways enrichment analysis. The cross pathways of compound-pathways and the diseases pathways of hyperuricemia from Comparative Toxicogenomics Database were be considered as the compound-disease pathways. Next, based on the compound-disease pathways and the PPI network, the core targets were identified based on the retrieved disease-genes. Finally, the compound-target-pathway-disease network was constructed by Cytoscape and the mechanism of Isobavachin anti-hyperuricemia was discussed based on the network analysis. Results: Our study demonstrated that there were five pathways involved in Isobavachin against hyperuricemia, including Drug metabolism-other enzymes, Metabolic pathways, Bile secretion, Renin-angiotensin system and Renin secretion. Among the proteins involved in these pathways, HPRT1, REN and ABCG2 were identified as the core targets associated with hyperuricemia, which regulated the five pathways mentioned above. It is quite different from that of Tranilast, which involved in the same pathways except Bile secretion instead of purine metabolism. Conclusion: This study revealed Isobavachin could regulate the pathways including Drug metabolism-other enzymes, Metabolic pathways, Bile secretion, Renin-angiotensin system, Renin secretion by core targets HPRT1, REN and ABCG2, in the treatment of hyperuricemia effect. Among them, the Bile secretion regulated by ABCG2 probably would be a novel pathway. Our work provided a theoretical basis for the pharmacological study of Isobavachin in lowering uric acid and further basic research.
An integrated in vitro/in silico approach to assess the anti-androgenic potency of Isobavachin
Food Chem Toxicol 2023 Apr 3;176:113764.PMID:37019376DOI:10.1016/j.fct.2023.113764.
Isobavachin is a dietary flavanone with multiple biological activities. Our previous research has confirmed the estrogenicity of Isobavachin, and this work aims to assess the anti-androgenic potency of Isobavachin by an integrated in vitro and in silico approach. Isobavachin can limit the proliferation of prostate cancer cells by inducing a distinct G1 cell-cycle arrest. In addition, Isobavachin also significantly represses the transcription of androgen receptor (AR)-downstream targets such as prostate specific antigen. Mechanistically, we demonstrated that Isobavachin can disrupt the nuclear translocation of AR and promote its proteasomal degradation. The results of computer simulations showed that Isobavachin can stably bind to AR, and the amino acid residue Gln711 may play a critical role in AR binding of both AR agonists and antagonists. In conclusion, this work has identified Isobavachin as a novel AR antagonist.
Pharmacological evaluation of a novel skeleton compound Isobavachin (4',7-dihydroxy-8-prenylflavanone) as a hypouricemic agent: Dual actions of URAT1/GLUT9 and xanthine oxidase inhibitory activity
Bioorg Chem 2023 Apr;133:106405.PMID:36753966DOI:10.1016/j.bioorg.2023.106405.
Previously we discovered a novel natural scaffold compound, Isobavachin (4', 7-dihydroxy-8-prenylflavanone), as a potent URAT1 inhibitor by shape and structure based on a virtue screening approach. In this study, further urate-lowering mechanism, pharmacokinetics and toxicities of Isobavachin were conducted. Isobavachin inhibited URAT1 with an IC50 value of 0.24 ± 0.06 μM, and residues S35, F365, I481 and R477 of URAT1 contributed to high affinity for Isobavachin. Isobavachin also inhibited glucose transporter 9 (GLUT9), another pivotal urate reabsorption transporter, with an IC50 value of 1.12 ± 0.26 μM. Molecular docking and MMGBSA results indicated that Isobavachin might compete residues R171, L75 and N333 with uric acid, which leads to inhibition of uric acid transport of GLUT9. Isobavachin weakly inhibited urate secretion transporters OAT1 with an IC50 value of 4.38 ± 1.27 μM, OAT3 with an IC50 of 3.64 ± 0.62 μM, and ABCG2 with an IC50 of 10.45 ± 2.17 μM. Isobavachin also inhibited xanthine oxidase (XOD) activity in vitro with an IC50 value of 14.43 ± 3.56 μM, and inhibited the hepatic XOD activities at 5-20 mg/kg in vivo. Docking and MMGBSA analysis indicated that Isobavachin might bind to the Mo-Pt catalyze center of XOD, which leads to inhibition of uric acid production. In vivo, Isobavachin exhibited powerful urate-lowering and uricosuric effects at 5-20 mg/kg compared with the positive drugs morin (20 mg/kg) and RDEA3170 (10 mg/kg). Safety assessments revealed that Isobavachin was safe and had no obvious toxicities. Isobavachin has little cell toxicity in HK2 cells as indicated by the MTT assay. In vivo, after treatment with 50 mg/kg Isobavachin for 14 days, Isobavachin had little renal toxicity, as revealed by serum CR/BUN levels, and no hepatotoxicity as revealed by ALT/AST levels. Further HE examination also suggests that Isobavachin has no obvious kidney/liver damage. A pharmacokinetic study in SD rats indicated Isobavachin had lower bioavailability (12.84 ± 5.13 %) but long half-time (7.04 ± 2.68 h) to maintain a continuous plasma concentration. Collectively, these results indicate that Isobavachin deserves further investigation as a candidate anti-hyperuricemic drug with a novel mechanism of action: selective urate reabsorption inhibitor (URAT1/GLUT9) with a moderate inhibitory effect on XOD.
Promoting effects of Isobavachin on neurogenesis of mouse embryonic stem cells were associated with protein prenylation
Acta Pharmacol Sin 2011 Apr;32(4):425-32.PMID:21441946DOI:10.1038/aps.2011.5.
Aim: Some small molecules can induce mouse embryonic stem (ES) cells to differentiate into neuronal cells. Here, we explored the effect of Isobavachin (IBA), a compound with a prenyl group at position 8 of ring A, on promoting neuronal differentiation and the potential role of its protein prenylation. Methods: The hanging drop method was employed for embryonic body (EB) formation to mimic embryo development in vivo. The EBs were treated with IBA at a final concentration of 10(-7) mol/L from EB stage (d 4) to d 8+10. Geranylgeranyltransferase I inhibitor GGTI-298 was subsequently used to disrupt protein prenylation. Neuronal subtypes, including neurons and astrocytes, were observed by fluorescence microscopy. Gene and protein expression levels were detected using RT-PCR and Western blot analysis, respectively. Results: With IBA treatment, nestin was highly expressed in the neural progenitors generated from EBs (d 4, d 8+0). EBs then further differentiated into neurons (marked by β-tubulin III) and astrocytes (marked by GFAP), which were both up-regulated in a time-dependent manner on d 8+5 and d 8+10. Co-treatment with GGTI-298 selectively abolished the IBA-induced neuronal differentiation. Moreover, in the MAPK pathway, p38 and JNK phosphorylation were down-regulated, while ERK phosphorylation was up-regulated after IBA treatment at different neuronal differentiation passages. Conclusion: IBA can facilitate mouse ES cells differentiating into neuronal cells. The mechanism involved protein prenylation and, subsequently, phos-ERK activation and the phos-p38 off pathway.