Ursolic acid acetate
(Synonyms: 熊果酸乙酸酯; Acetylursolic acid; 3-Acetylursolic acid) 目录号 : GC37872
A triterpene with diverse biological activities
Cas No.:7372-30-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
3-Acetylursolic acid is a triterpene and derivative of ursolic acid with diverse biological activities.1,2,3 It inhibits ADP-, thrombin-, or epinephrine-induced aggregation of isolated rat platelets (IC50s = <1, 0.8, and <1 mg/ml, respectively).1 3-Acetylursolic acid is active against P. falciparum in vitro (IC50 = 4 ?M).2 It is also active against B. cereus, S. aureus, and S. pneumoniae (MICs = 39.1, 19.6, and 4.81 ?M, respectively).3 It is cytotoxic to HepG2 cells (LC50 = 351 ?M).
1.Habila, J.D., Shode, F.O., and Opoku, A.R.Triterpenoids from Eucalyptus grandis hill ex maiden inhibits platelet aggregationAfr. J. Microbiol. Res.5(26)4646-4651(2011) 2.Innocente, A.M., Silva, G.N.S., Cruz, L.N., et al.Synthesis and antiplasmodial activity of betulinic acid and ursolic acid analoguesMolecules17(10)12003-12014(2012) 3.Setzer, W.N., Setzer, M.C., Bates, R.B., et al.Biologically active triterpenoids of Syncarpia glomulifera bark extract from Paluma, North Queensland, AustraliaPlanta Med.66(2)176-177(2000)
| Cas No. | 7372-30-7 | SDF | |
| 别名 | 熊果酸乙酸酯; Acetylursolic acid; 3-Acetylursolic acid | ||
| Canonical SMILES | C[C@]12[C@]3(C([C@@]4([H])[C@](C(O)=O)(CC[C@@H](C)[C@@H]4C)CC3)=CC[C@]1([H])[C@@]5([C@@](C(C)([C@@H](OC(C)=O)CC5)C)([H])CC2)C)C | ||
| 分子式 | C32H50O4 | 分子量 | 498.74 |
| 溶解度 | DMF: 15 mg/ml,Ethanol: 1 mg/ml | 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 | 2.0051 mL | 10.0253 mL | 20.0505 mL |
| 5 mM | 0.401 mL | 2.0051 mL | 4.0101 mL |
| 10 mM | 0.2005 mL | 1.0025 mL | 2.0051 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。
Evaluating Iso-Mukaadial Acetate and Ursolic acid acetate as Plasmodium falciparum Hypoxanthine-Guanine-Xanthine Phosphoribosyltransferase Inhibitors
Biomolecules 2019 Dec 11;9(12):861.PMID:31835879DOI:10.3390/biom9120861.
To date, Plasmodium falciparum is one of the most lethal strains of the malaria parasite. P. falciparum lacks the required enzymes to create its own purines via the de novo pathway, thereby making Plasmodium falciparum hypoxanthine-guanine-xanthine phosphoribosyltransferase (PfHGXPT) a crucial enzyme in the malaria life cycle. Recently, studies have described iso-mukaadial acetate and Ursolic acid acetate as promising antimalarials. However, the mode of action is still unknown, thus, the current study sought to investigate the selective inhibitory and binding actions of iso-mukaadial acetate and Ursolic acid acetate against recombinant PfHGXPT using in-silico and experimental approaches. Recombinant PfHGXPT protein was expressed using E. coli BL21 cells and homogeneously purified by affinity chromatography. Experimentally, iso-mukaadial acetate and Ursolic acid acetate, respectively, demonstrated direct inhibitory activity towards PfHGXPT in a dose-dependent manner. The binding affinity of iso-mukaadial acetate and Ursolic acid acetate on the PfHGXPT dissociation constant (KD), where it was found that 0.0833 µM and 2.8396 µM, respectively, are indicative of strong binding. The mode of action for the observed antimalarial activity was further established by a molecular docking study. The molecular docking and dynamics simulations show specific interactions and high affinity within the binding pocket of Plasmodium falciparum and human hypoxanthine-guanine phosphoribosyl transferases. The predicted in silico absorption, distribution, metabolism and excretion/toxicity (ADME/T) properties predicted that the iso-mukaadial acetate ligand may follow the criteria for orally active drugs. The theoretical calculation derived from ADME, molecular docking and dynamics provide in-depth information into the structural basis, specific bonding and non-bonding interactions governing the inhibition of malarial. Taken together, these findings provide a basis for the recommendation of iso-mukaadial acetate and Ursolic acid acetate as high-affinity ligands and drug candidates against PfHGXPT.
Iso-mukaadial acetate and Ursolic acid acetate inhibit the chaperone activity of Plasmodium falciparum heat shock protein 70-1
Cell Stress Chaperones 2021 Jul;26(4):685-693.PMID:34023985DOI:10.1007/s12192-021-01212-6.
Plasmodium falciparum is the most lethal malaria parasite. The present study investigates the interaction capabilities of select plant derivatives, iso-mukaadial acetate (IMA) and Ursolic acid acetate (UAA), against P. falciparum Hsp70-1 (PfHsp70-1) using in vitro approaches. PfHsp70-1 facilitates protein folding in the parasite and is deemed a prospective antimalarial drug target. Recombinant PfHsp70-1 protein was expressed in E. coli BL21 cells and homogeneously purified by affinity chromatography. The interaction between the compounds and PfHsp70-1 was evaluated using malate dehydrogenase (MDH), and luciferase aggregation assay, ATPase activity assay, and Fourier transform infrared (FTIR). PfHsp70-1 prevented the heat-induced aggregation of MDH and luciferase. However, the PfHsp70-1 chaperone role was inhibited by IMA or UAA, leading to both MDH and luciferase's thermal aggregation. The basal ATPase activity of PfHsp70-1 (0.121 nmol/min/mg) was closer to UAA (0.131 nmol/min/mg) (p = 0.0675) at 5 mM compound concentration, suggesting that UAA has no effect on PfHsp70-1 ATPase activity. However, ATPase activity inhibition was similar between IMA (0.068 nmol/min/mg) (p < 0.0001) and polymyxin B (0.083 nmol/min/mg) (p < 0.0001). The lesser the Pi values, the lesser ATP hydrolysis observed due to compound binding to the ATPase domain. FTIR spectra analysis of IMA and UAA resulted in PfHsp70-1 structural alteration for β-sheets shifting the amide I band from 1637 cm-1 to 1639 cm-1, and for α-helix from 1650 cm-1 to 1652 cm-1, therefore depicting secondary structural changes with an increase in secondary structure percentage suggesting that these compounds interact with PfHsp70-1.
Ursolic acid as a potential inhibitor of Mycobacterium tuberculosis cytochrome bc1 oxidase-a molecular modelling perspective
J Mol Model 2022 Jan 13;28(2):35.PMID:35022913DOI:10.1007/s00894-021-04993-w.
The escalating burden of tuberculosis disease and drastic effects of current medicine has stimulated a search for alternative drugs. A medicinal plant Warburgia salutaris has been reported to possess inhibitory properties against M. tuberculosis. In this study, we apply computational methods to investigate the probability of W. salutaris compounds as potential inhibitors of M. tuberculosis QcrB protein. We performed molecular docking, molecular dynamics simulations, radius of gyration, principal component analysis (PCA), and molecular mechanics-generalized born surface area (MM-GBSA) binding-free energy calculations in explicit solvent to achieve our objective. The results suggested that ursolic acid (UA) and Ursolic acid acetate (UAA) could serve as preferred potential inhibitors of mycobacterial QcrB compared to lansoprazole sulphide (LSPZ) and telacebec (Q203)-UA and UAA have a higher binding affinity to QcrB compared to LSPZ and Q203 drugs. UA binding affinity is attributed to hydrogen bond formation with Val120, Arg364 and Arg366, and largely resonated from van der Waals forces resulting from UA interactions with hydrophobic amino acids in its vicinity. UAA binds to the porphyrin ring binding site with higher binding affinity compared to LSPZ. The binding affinity results primarily from van der Waals forces between UAA and hydrophobic residues of QcrB in the porphyrin ring binding site where UAA binds competitively. UA and UAA formed stable complexes with the protein with reduced overall residue mobility, consequently supporting the magnitude of binding affinity of the respective ligands. UAA could potentially compete with the porphyrin ring for the binding site and deprive the mycobacterial cell from oxygen, consequently disturbing mycobacterial oxygen-dependent metabolic processes. Therefore, discovery of a compound that competes with porphyrin ring for the binding site may be useful in QcrB pharmocological studies. UA proved to be a superior compound, although its estimated toxicity profile revealed UA to be hepatotoxic within acceptable parameters. Although preliminary findings of this report still warrant experimental validation, they could serve as a baseline for the development of new anti-tubercular drugs from natural resources that target QcrB.