(4α)-17-hydroxy-Kauran-18-oic acid
* Please be kindly noted products are not for therapeutic use. We do not sell to patients.
| Category | Others |
| Catalog number | BBF-05470 |
| CAS | 58691-64-8 |
| Molecular Weight | 320.47 |
| Molecular Formula | C20H32O3 |
Online Inquiry
Specification
| Synonyms | (-)-17-Hydroxy-16alpha-kauran-19-oic acid; Kauran-18-oic acid, 17-hydroxy-, (4α)-; Kauran-18-oic acid, 17-hydroxy-, (4alpha)-; (1S,4S,5R,9S,10R,13R,14S)-14-(hydroxymethyl)-5,9-dimethyltetracyclo[11.2.1.01,10.04,9]hexadecane-5-carboxylic acid; 17-Hydroxykaura-18-oic acid |
| IUPAC Name | (4R,4aS,6aS,8S,9R,11aR,11bS)-8-(hydroxymethyl)-4,11b-dimethyltetradecahydro-6a,9-methanocyclohepta[a]naphthalene-4-carboxylic acid |
| Canonical SMILES | CC12CCCC(C1CCC34C2CCC(C3)C(C4)CO)(C)C(=O)O |
| InChI | InChI=1S/C20H32O3/c1-18-7-3-8-19(2,17(22)23)15(18)6-9-20-10-13(4-5-16(18)20)14(11-20)12-21/h13-16,21H,3-12H2,1-2H3,(H,22,23)/t13-,14-,15+,16+,18-,19-,20+/m1/s1 |
| InChI Key | HHAMKMUMKLXDFQ-GVUXFJDWSA-N |
Properties
| Boiling Point | 469.1±18.0°C at 760 mmHg |
| Density | 1.2±0.1 g/cm3 |
Reference Reading
1. Hepatocytic Activating Transcription Factor 3 Protects Against Steatohepatitis via Hepatocyte Nuclear Factor 4α
Yanyong Xu, Shuwei Hu, Kavita Jadhav, Yingdong Zhu, Xiaoli Pan, Fathima Cassim Bawa, Liya Yin, Yanqiao Zhang Diabetes. 2021 Nov;70(11):2506-2517. doi: 10.2337/db21-0181. Epub 2021 Sep 2.
Activating transcription factor 3 (ATF3) has been shown to play an important role in HDL metabolism; yet, the role of hepatocytic ATF3 in the development of steatohepatitis remains elusive. Here we show that adenoassociated virus-mediated overexpression of human ATF3 in hepatocytes prevents diet-induced steatohepatitis in C57BL/6 mice and reverses steatohepatitis in db/db mice. Conversely, global or hepatocyte-specific loss of ATF3 aggravates diet-induced steatohepatitis. Mechanistically, hepatocytic ATF3 induces hepatic lipolysis and fatty acid oxidation and inhibits inflammation and apoptosis. We further show that hepatocyte nuclear factor 4α (HNF4α) is required for ATF3 to improve steatohepatitis. Thus, the current study indicates that ATF3 protects against steatohepatitis through, at least in part, hepatic HNF4α. Targeting hepatic ATF3 may be useful for treatment of steatohepatitis.
2. Hepatocyte ATF3 protects against atherosclerosis by regulating HDL and bile acid metabolism
Yanyong Xu, Yuanyuan Li, Kavita Jadhav, Xiaoli Pan, Yingdong Zhu, Shuwei Hu, Shaoru Chen, Liuying Chen, Yong Tang, Helen H Wang, Ling Yang, David Q-H Wang, Liya Yin, Yanqiao Zhang Nat Metab. 2021 Jan;3(1):59-74. doi: 10.1038/s42255-020-00331-1. Epub 2021 Jan 18.
Activating transcription factor (ATF)3 is known to have an anti-inflammatory function, yet the role of hepatic ATF3 in lipoprotein metabolism or atherosclerosis remains unknown. Here we show that overexpression of human ATF3 in hepatocytes reduces the development of atherosclerosis in Western-diet-fed Ldlr-/- or Apoe-/- mice, whereas hepatocyte-specific ablation of Atf3 has the opposite effect. We further show that hepatic ATF3 expression is inhibited by hydrocortisone. Mechanistically, hepatocyte ATF3 enhances high-density lipoprotein (HDL) uptake, inhibits intestinal fat and cholesterol absorption and promotes macrophage reverse cholesterol transport by inducing scavenger receptor group B type 1 (SR-BI) and repressing cholesterol 12α-hydroxylase (CYP8B1) in the liver through its interaction with p53 and hepatocyte nuclear factor 4α, respectively. Our data demonstrate that hepatocyte ATF3 is a key regulator of HDL and bile acid metabolism and atherosclerosis.
3. Hepatocyte Nuclear Factor 4α Prevents the Steatosis-to-NASH Progression by Regulating p53 and Bile Acid Signaling (in mice)
Yanyong Xu, Yingdong Zhu, Shuwei Hu, Yang Xu, Diane Stroup, Xiaoli Pan, Fathima Cassim Bawa, Shaoru Chen, Raja Gopoju, Liya Yin, Yanqiao Zhang Hepatology. 2021 Jun;73(6):2251-2265. doi: 10.1002/hep.31604. Epub 2021 May 14.
Background and aims: Hepatocyte nuclear factor 4α (HNF4α) is highly enriched in the liver, but its role in the progression of nonalcoholic liver steatosis (NAFL) to NASH has not been elucidated. In this study, we investigated the effect of gain or loss of HNF4α function on the development and progression of NAFLD in mice. Approach and results: Overexpression of human HNF4α protected against high-fat/cholesterol/fructose (HFCF) diet-induced steatohepatitis, whereas loss of Hnf4α had opposite effects. HNF4α prevented hepatic triglyceride accumulation by promoting hepatic triglyceride lipolysis, fatty acid oxidation, and VLDL secretion. Furthermore, HNF4α suppressed the progression of NAFL to NASH. Overexpression of human HNF4α inhibited HFCF diet-induced steatohepatitis in control mice but not in hepatocyte-specific p53-/- mice. In HFCF diet-fed mice lacking hepatic Hnf4α, recapitulation of hepatic expression of HNF4α targets cholesterol 7α-hydroxylase and sterol 12α-hydroxylase and normalized hepatic triglyceride levels and attenuated steatohepatitis. Conclusions: The current study indicates that HNF4α protects against diet-induced development and progression of NAFLD by coordinating the regulation of lipolytic, p53, and bile acid signaling pathways. Targeting hepatic HNF4α may be useful for treatment of NASH.
Recommended Products
| BBF-03755 | Actinomycin D | Inquiry |
| BBF-01826 | Deoxymannojirimycin | Inquiry |
| BBF-01829 | Deoxynojirimycin | Inquiry |
| BBF-03754 | CASTANOSPERMINE | Inquiry |
| BBF-03753 | Baicalin | Inquiry |
| BBF-01693 | Doxorubicin EP Impurity A (Daunorubicin) | Inquiry |
Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
