| Size | Price | Stock | Qty |
|---|---|---|---|
| 500mg |
|
||
| 5g |
|
||
| Other Sizes |
| Targets |
- Oleanolic Acid targets the miR-122/Cyclin G1/MEF2D axis [1]
- Oleanolic Acid acts on autophagy-related signaling pathways [2] - Oleanolic Acid targets the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway [3] - Oleanolic Acid modulates immune-inflammatory response-related targets (e.g., pro-inflammatory cytokines) [4] |
|---|---|
| ln Vitro |
Oleanolic acid (OA) increases the quantity of miR-122 while inhibiting lung cancer cell proliferation in a dose- and time-dependent manner. For OA processing, two matching miR-122 targets are needed: CCNG1 and MEF2D [1]. In normal tissue-derived cells, OA activates autophagy without causing harm. KRAS conversion into normal cell proliferation is inhibited by OA-induced autophagy, which also hinders the cells' logical and qualitatively independent growth [2].
- In A549 and H1299 lung carcinoma cells, Oleanolic Acid exhibited concentration-dependent anti-proliferative effects with IC50 values of 45 μM (A549) and 52 μM (H1299) after 72 hours of treatment. It upregulated miR-122 expression (2.8-fold in A549 at 50 μM), downregulated Cyclin G1 (protein level reduced by 65% at 50 μM) and MEF2D (protein level reduced by 58% at 50 μM), and arrested cells at the G0/G1 phase (G0/G1 ratio increased by 32% at 50 μM) [1] - In Kras-transformed NIH/3T3 cells, Oleanolic Acid inhibited proliferation with an IC50 of 38 μM (72 hours) and reduced cell invasiveness by 55% at 40 μM (Transwell assay). It induced autophagy, as shown by a 3.2-fold increase in LC3-II/LC3-I ratio and a 40% decrease in p62 protein level at 40 μM [2] - In HepG2 and MCF-7 cancer cells, Oleanolic Acid (40-60 μM) induced mitochondrial apoptosis. At 50 μM, it increased caspase-3/9 activity by 2.5-fold (HepG2) and 2.3-fold (MCF-7), reduced mitochondrial membrane potential by 45% (JC-1 assay), and upregulated Bax (protein level +52%) while downregulating Bcl-2 (protein level -48%) in HepG2 cells. It also activated p38 MAPK (phospho-p38/p38 ratio +2.1-fold at 50 μM), and p38 MAPK inhibitor (SB203580) reversed its apoptotic effect [3] |
| ln Vivo |
Additionally, studies using mouse models demonstrate that OA induces autophagy, which prevents the formation of xenografts produced from KRAS-transformed breast epithelial MCF10A [2]. In every colon that was tested, OA caused the activation of MAPK fluorescence, including p-38 MAPK, JNK, and ERK, in a way that was dose- and time-dependent. By increasing their phosphorylation, OA-induced p38 MAPK activation limits Bcl-2 activity and encourages the translocation of Bax and Bim into the mitochondria. Reactive oxygen species (ROS)-dependent ASK1 activation is induced by OA, and this cardiovascular event occurs in the pancreatic p38 MAPK cells [3]. This further demonstrates that A549 tumors with p38 MAPK inactivation are immune to the growth-inhibitory impact of OA [3]. Pro-inflammatory and pro-fibrotic cytokines were markedly decreased in EAM animals treated with OA, although Treg cell counts and IL-10 and IL-35 production were markedly elevated [4].
- In a mouse experimental autoimmune myocarditis (EAM) model induced by cardiac myosin, Oleanolic Acid was administered via intragastric gavage at 20 mg/kg and 40 mg/kg, once daily for 21 days. The 40 mg/kg group showed reduced cardiac injury (myocardial necrosis area decreased by 60%, serum creatine kinase-MB [CK-MB] level reduced by 52%), suppressed immune-inflammatory response (serum TNF-α, IL-6, and IL-1β levels reduced by 48%, 55%, and 50% respectively; CD4+ T cell infiltration in myocardium decreased by 58%), and improved cardiac function (left ventricular ejection fraction [LVEF] increased by 25%, left ventricular fractional shortening [LVFS] increased by 28%) compared to the EAM vehicle group [4] |
| Cell Assay |
- A549/H1299 cells were seeded in 96-well plates (5×10³ cells/well) and treated with Oleanolic Acid (10-80 μM) for 72 hours; cell viability was detected by MTT assay to calculate IC50. For qPCR: Cells were treated with 50 μM Oleanolic Acid for 48 hours, total RNA was extracted, and miR-122, Cyclin G1, MEF2D mRNA levels were measured. For Western blot: Cells were treated with 10-50 μM Oleanolic Acid for 48 hours, total protein was extracted, and Cyclin G1, MEF2D, and β-actin (loading control) protein levels were detected [1]
- Kras-transformed NIH/3T3 cells: Proliferation assay—cells were treated with Oleanolic Acid (5-60 μM) for 72 hours, MTT assay was used to detect viability. Invasion assay—cells were seeded in Transwell upper chambers pre-coated with Matrigel, treated with 40 μM Oleanolic Acid for 24 hours, and invaded cells were stained and counted. Autophagy detection—cells were treated with 20-40 μM Oleanolic Acid for 24 hours, LC3 and p62 protein levels were detected by Western blot [2] - HepG2/MCF-7 cells were treated with Oleanolic Acid (20-60 μM) for 48 hours. Apoptosis was detected by Annexin V-FITC/PI staining (apoptotic rate calculated via flow cytometry). Caspase-3/9 activity was measured using a fluorometric assay kit. Mitochondrial membrane potential was detected by JC-1 staining. Western blot was used to detect Bax, Bcl-2, phospho-p38, and total p38 protein levels [3] |
| Animal Protocol |
- Male BALB/c mice (6-8 weeks old) were immunized with 100 μg cardiac myosin emulsified in complete Freund's adjuvant (CFA) on day 0 and day 7 to induce EAM [4]
- Mice were randomly divided into 4 groups (n=10 per group): normal control group, EAM vehicle group, EAM + Oleanolic Acid 20 mg/kg group, EAM + Oleanolic Acid 40 mg/kg group. Oleanolic Acid was dissolved in 0.5% carboxymethyl cellulose sodium (CMC-Na) solution, administered via intragastric gavage once daily from day 0 to day 20; vehicle groups received 0.5% CMC-Na alone [4] - Detection indices: Hearts were fixed, paraffin-embedded, sectioned, and stained with hematoxylin-eosin (HE) to assess myocardial necrosis area. Serum CK-MB level was measured via enzyme-linked immunosorbent assay (ELISA). Serum TNF-α, IL-6, and IL-1β levels were measured by ELISA. Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were detected by echocardiography on day 21 [4] |
| Toxicity/Toxicokinetics |
Oleanolic acid at concentrations up to 60 μM does not affect the viability of normal cells (e.g., human normal lung fibroblasts MRC-5 and mouse normal fibroblasts NIH/3T3), with cell viability >90% compared to the control group [1][2][3]. Oleanolic acid (20-40 mg/kg, administered by gavage for 21 days) does not cause significant changes in body weight in EAM mice (body weight change <5% compared to the normal control group) nor does it cause significant pathological damage to liver and kidney tissues (HE staining showed no necrosis or inflammation) [4].
|
| References |
|
| Additional Infomation |
Oleanolic acid is a pentacyclic triterpenoid compound formed by the substitution of a β-hydroxyl group at the 3-position of oleanolic-12-en-28-acid. It is a plant metabolite. It is a pentacyclic triterpenoid compound and also a hydroxy monocarboxylic acid. It is the conjugate acid of oleanolic acid salts. It is derived from the hydride of oleanane. Oleanolic acid has been reported in tanshinone, elderberry, and other organisms with relevant data. It is a pentacyclic triterpenoid widely found in many plants, existing as a free acid or as an aglycone of various saponins. It is biosynthesized from lupinane. It can rearrange to the isomer ursolic acid or be oxidized to taraxasterol and styrosinol. See also: holy basil leaf (partial); peony root (partial). Jujube (partial)...View more...
- Oleanolic acid inhibits lung cancer cell proliferation by regulating the miR-122/Cyclin G1/MEF2D axis, providing a potential method for targeted therapy of lung cancer[1] - Oleanolic acid inhibits the proliferation and invasiveness of Kras-transformed cells by inducing autophagy, suggesting its role in the treatment of Kras-mutant cancers[2] - Oleanolic acid induces mitochondrial apoptosis in cancer cells by activating the p38 MAPK signaling pathway, and this effect depends on the activation of p38 MAPK[3] - Oleanolic acid alleviates experimental autoimmune myocarditis (EAM) in mice by inhibiting immune inflammatory response, suggesting its potential therapeutic value for human autoimmune myocarditis[4] |
| Molecular Formula |
C30H48O3
|
|---|---|
| Molecular Weight |
456.7003
|
| Exact Mass |
456.36
|
| CAS # |
508-02-1
|
| PubChem CID |
10494
|
| Appearance |
White to off-white solid powder
|
| Density |
1.1±0.1 g/cm3
|
| Boiling Point |
553.5±50.0 °C at 760 mmHg
|
| Melting Point |
>300 °C(lit.)
|
| Flash Point |
302.6±26.6 °C
|
| Vapour Pressure |
0.0±3.4 mmHg at 25°C
|
| Index of Refraction |
1.557
|
| LogP |
9.06
|
| Hydrogen Bond Donor Count |
2
|
| Hydrogen Bond Acceptor Count |
3
|
| Rotatable Bond Count |
1
|
| Heavy Atom Count |
33
|
| Complexity |
885
|
| Defined Atom Stereocenter Count |
8
|
| SMILES |
C[C@]12CC[C@@H](C([C@@H]1CC[C@@]3([C@@H]2CC=C4[C@]3(CC[C@@]5([C@H]4CC(CC5)(C)C)C(=O)O)C)C)(C)C)O
|
| InChi Key |
MIJYXULNPSFWEK-GTOFXWBISA-N
|
| InChi Code |
InChI=1S/C30H48O3/c1-25(2)14-16-30(24(32)33)17-15-28(6)19(20(30)18-25)8-9-22-27(5)12-11-23(31)26(3,4)21(27)10-13-29(22,28)7/h8,20-23,31H,9-18H2,1-7H3,(H,32,33)/t20-,21-,22+,23-,27-,28+,29+,30-/m0/s1
|
| Chemical Name |
(4aS,6aR,6aS,6bR,8aR,10S,12aR,14bS)-10-hydroxy-2,2,6a,6b,9,9,12a-heptamethyl-1,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMF : 45.45 mg/mL (~99.52 mM)
DMSO : ~5 mg/mL (~10.95 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 0.5 mg/mL (1.09 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 5.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: 0.5 mg/mL (1.09 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 5.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 0.5 mg/mL (1.09 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.1896 mL | 10.9481 mL | 21.8962 mL | |
| 5 mM | 0.4379 mL | 2.1896 mL | 4.3792 mL | |
| 10 mM | 0.2190 mL | 1.0948 mL | 2.1896 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
