Betulinic acid

Anti-HIV and antitumor compound,pentacyclic triterpenoid CAS# 472-15-1

Betulinic acid

Catalog No. BCN5524----Order now to get a substantial discount!

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Quality Control of Betulinic acid

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Chemical structure

Betulinic acid

3D structure

Chemical Properties of Betulinic acid

Cas No. 472-15-1 SDF Download SDF
PubChem ID 64971 Appearance White powder
Formula C30H48O3 M.Wt 456.7
Type of Compound Triterpenoids Storage Desiccate at -20°C
Synonyms Lupatic acid; Betulic acid
Solubility DMSO : 60 mg/mL (131.38 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
Chemical Name (1R,3aS,5aR,5bR,7aR,9S,11aR,11bR,13aR,13bR)-9-hydroxy-5a,5b,8,8,11a-pentamethyl-1-prop-1-en-2-yl-1,2,3,4,5,6,7,7a,9,10,11,11b,12,13,13a,13b-hexadecahydrocyclopenta[a]chrysene-3a-carboxylic acid
SMILES CC(=C)C1CCC2(C1C3CCC4C5(CCC(C(C5CCC4(C3(CC2)C)C)(C)C)O)C)C(=O)O
Standard InChIKey QGJZLNKBHJESQX-FZFNOLFKSA-N
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Betulinic acid

1 Aleurites sp. 2 Arbutus sp. 3 Betula sp. 4 Castanea sp. 5 Ceanothus sp. 6 Centella sp. 7 Cornus sp. 8 Eryngium sp. 9 Glycyrrhiza sp. 10 Gratiola sp. 11 Gypsophila sp. 12 Harungana sp. 13 Hydnocarpus sp. 14 Lavandula sp. 15 Melaleuca sp. 16 Melissa sp. 17 Menyanthes sp. 18 Morus sp. 19 Nerium sp. 20 Olea sp. 21 Origanum sp. 22 Phyllanthus sp. 23 Platanus sp. 24 Punica sp. 25 Sanguisorba sp. 26 Syzygium sp. 27 Viscum sp.

Biological Activity of Betulinic acid

DescriptionBetulinic acid is a natural pentacyclic triterpenoid, acts as a eukaryotic topoisomerase I inhibitor, with an IC50 of 5 μM, and possesses anti-HIV, anti-malarial, immunomodulatory, anti-inflammatory and anti-tumor properties.Betulinic acid is a selective inducer of apoptosis in tumor cells, it inhibits activation of NF-kappaB and NF-kappaB-regulated gene expression induced by carcinogens and inflammatory stimuli.
TargetsHBV | HIV | MMP(e.g.TIMP) | TNF-α | MEK | ERK | PI3K | Akt | NF-kB | IL Receptor | COX | p65
In vitro

Betulinic acid, a bioactive pentacyclic triterpenoid, inhibits skeletal-related events induced by breast cancer bone metastases and treatment.[Pubmed: 24463094]

Toxicol Appl Pharmacol. 2014 Mar 1;275(2):152-62.

The present study provides evidence on the protective and therapeutic potential of Betulinic acid on cancer-associated bone diseases. Betulinic acid is a naturally occurring triterpenoid with the beneficial activity to limit the progression and severity of cancer, diabetes, cardiovascular diseases, atherosclerosis, and obesity.
METHODS AND RESULTS:
We first investigated its effect on breast cancer cells, osteoblastic cells, and osteoclasts in the vicious cycle of osteolytic bone metastasis. Betulinic acid reduced cell viability and the production of parathyroid hormone-related protein (PTHrP), a major osteolytic factor, in MDA-MB-231 human metastatic breast cancer cells stimulated with or without tumor growth factor-β. Betulinic acid blocked an increase in the receptor activator of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin ratio by downregulating RANKL protein expression in PTHrP-treated human osteoblastic cells. In addition, Betulinic acid inhibited RANKL-induced osteoclastogenesis in murine bone marrow macrophages and decreased the production of resorbed area in plates with a bone biomimetic synthetic surface by suppressing the secretion of matrix metalloproteinase (MMP)-2, MMP-9, and cathepsin K in RANKL-induced osteoclasts. Furthermore, oral administration of Betulinic acid inhibited bone loss in mice intra-tibially inoculated with breast cancer cells and in ovariectomized mice causing estrogen deprivation, as supported by the restored bone morphometric parameters and serum bone turnover markers.
CONCLUSIONS:
Taken together, these findings suggest that Betulinic acid may have the potential to prevent bone loss in patients with bone metastases and cancer treatment-induced estrogen deficiency.

Increase of betulinic acid production in Saccharomyces cerevisiae by balancing fatty acids and betulinic acid forming pathways.[Pubmed: 24389702]

Appl Microbiol Biotechnol. 2014 Apr;98(7):3081-9.

Betulinic acid is a plant-based triterpenoid that has been recognized for its antitumor and anti-HIV activities. The level of Betulinic acid in its natural hosts is extremely low.
METHODS AND RESULTS:
In the present study, we constructed Betulinic acid biosynthetic pathway in Saccharomyces cerevisiae by metabolic engineering. Given the Betulinic acid forming pathways sharing the common substrate acetyl-CoA with fatty acid synthesis, the metabolic fluxes between the two pathways were varied by changing gene expressions, and their effects on Betulinic acid production were investigated. We constructed nine S. cerevisiae strains representing nine combinations of the flux distributions between Betulinic acid and fatty acid pathways. Our results demonstrated that it was possible to improve the Betulinic acid production in S. cerevisiae while keeping a desirable growth phenotype by optimally balancing the carbon fluxes of the two pathways. Through modulating the expressions of the key genes on Betulinic acid and fatty acid pathways, the difference in Betulinic acid yield varied largely in the range of 0.01-1.92 mg L(-1) OD(-1).
CONCLUSIONS:
The metabolic engineering approach used in this study could be extended for synthesizing other triterpenoids in S. cerevisiae.

Protocol of Betulinic acid

Kinase Assay

Betulinic acid suppresses carcinogen-induced NF-kappa B activation through inhibition of I kappa B alpha kinase and p65 phosphorylation: abrogation of cyclooxygenase-2 and matrix metalloprotease-9.[Pubmed: 12960358]

Betulinic acid isolated from Vitis amurensis root inhibits 3-isobutyl-1-methylxanthine induced melanogenesis via the regulation of MEK/ERK and PI3K/Akt pathways in B16F10 cells.[Pubmed: 24632067]

Food Chem Toxicol. 2014 Jun;68:38-43.

Previously, Betulinic acid was identified as one of the main compounds responsible for the anti-melanogenic effect in Vitis amurensis root.
METHODS AND RESULTS:
In this study, we investigated the precise mechanism underlying the anti-melanogenic activity of Betulinic acid in B16F10 cells. Betulinic acid significantly attenuated 3-isobutyl-1-methylxanthine (IBMX)-induced melanin production by inhibiting tyrosinase, tyrosinase related protein (TRP)-1, and TRP-2 expression through the modulation of their corresponding transcription factors, microphthalamia associated transcription factor (MITF) and cAMP response element binding protein (CREB), in B16F10 cells. In addition, phosphorylation of mitogen-activated protein kinase kinase (MEK)/extracellular regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/Akt, involved in the melanogenic processes, were ameliorated by Betulinic acid treatment. Role of MEK/ERK and PI3K/Akt signaling pathway in the melanogenesis was confirmed by using specific inhibitors, PD98059 (for MEK/ERK) and LY294002 (for PI3K/Akt), respectively. As a result, Betulinic acid inhibited melanin production by tyrosinase, TRP-1, and TRP-2 inhibition through the regulation of CREB and MITF, which was accompanied with MEK/ERK and PI3K/Akt inactivation in IBMX-stimulated B16F10 cells.
CONCLUSIONS:
Consequently, these results demonstrate a novel molecular function of Betulinic acid derived from V. amurensis root in melanogenesis, which in turn enhances our understanding on the application of cosmetic therapy for reducing skin hyperpigmentation.

J Immunol. 2003 Sep 15;171(6):3278-86.

Betulinic acid (BA), a pentacyclic triterpene isolated from the bark of the white birch tree, has been reported to be a selective inducer of apoptosis in tumor cells. It also exhibits anti-inflammatory and immunomodulatory properties. How BA mediates these effects is not known. Because of the critical role of the transcription factor NF-kappaB in growth modulatory, inflammatory, and immune responses, we postulated that BA modulates the activity of this factor.
METHODS AND RESULTS:
In this study we investigated the effect of BA on NF-kappaB and NF-kappaB-regulated gene expression activated by a variety of inflammatory and carcinogenic agents. BA suppressed NF-kappaB activation induced by TNF, PMA, cigarette smoke, okadaic acid, IL-1, and H(2)O(2). The suppression of NF-kappaB activation was not cell-type specific. BA suppressed the activation of IkappaBalpha kinase, thus abrogating the phosphorylation and degradation of IkappaBalpha. We found that BA inhibited NF-kappaB activated by TNFR 1, TNFR-associated death domain, TNFR-associated factor 2, NF-kappaB-inducing kinase, and IkappaBalpha kinase. Treatment of cells with this triterpinoid also suppressed NF-kappaB-dependent reporter gene expression and the production of NF-kappaB-regulated gene products such as cyclooxygenase-2 and matrix metaloproteinase-9 induced by inflammatory stimuli. Furthermore, BA enhanced TNF-induced apoptosis.
CONCLUSIONS:
Overall, our results indicated that BA inhibits activation of NF-kappaB and NF-kappaB-regulated gene expression induced by carcinogens and inflammatory stimuli. This may provide a molecular basis for the ability of BA to mediate apoptosis, suppress inflammation, and modulate the immune response.

Animal Research

Research on HBV DNA inhibition of plasmid acute infection mouse with betulinic acid[Pubmed: 24956858]

Zhongguo Zhong Yao Za Zhi. 2014 Mar;39(6):1097-100.

Betulinic acid is a naturally occurring pentacyclic triterpenoid, which has antiretroviral, antimalarial, and anti-inflammatory properties. The purpose of this study is to investigate the HBV DNA replication inhibition in the mouse model with Betulinic acid.
METHODS AND RESULTS:
Hydrodynamic injection method via the tail vein with the Paywl. 3 plasmid was used to establish the animal mode (n = 15), and the mice were randomly divided into the PBS control group (n = 5), Betulinic acid treatment group (n = 5) and lamivudine control group (n = 5). The day after successful modeling , the mice would have taken Betulinic acid (100 mg x kg(-1)), lamivudine (50 mg x kg(-1)), PBS drugs orally, once daily for 7 days, blood samples were acquired from the orbital venous blood at 3, 5, 7 days after the administering, HBsAg and HBeAg in serum concentration were measured by ELISA and the mice were sacrificed after 7 days, HBV DNA southern detections were used with part of mice livers. The results showed that Betulinic acid significantly inhibited the expression of HbsAg in the mice model at the fifth day compared with the control group, and there was no significant differences between the effects of lamivudine and the PBS control group; both the Betulinic acid and lamivudine groups had no significant inhibition for the HBeAg expression; the HBV DNA expressions of the liver tissue from the Betulinic acid and lamivudine groups were inhibited compared with the control group.
CONCLUSIONS:
Taken together, these results reveal Betulinic acid can inhibit the HBsAg expression and replication of the liver HBV DNA in the mouse model.

Betulinic acid Dilution Calculator

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Preparing Stock Solutions of Betulinic acid

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.1896 mL 10.9481 mL 21.8962 mL 43.7924 mL 54.7405 mL
5 mM 0.4379 mL 2.1896 mL 4.3792 mL 8.7585 mL 10.9481 mL
10 mM 0.219 mL 1.0948 mL 2.1896 mL 4.3792 mL 5.4741 mL
50 mM 0.0438 mL 0.219 mL 0.4379 mL 0.8758 mL 1.0948 mL
100 mM 0.0219 mL 0.1095 mL 0.219 mL 0.4379 mL 0.5474 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Betulinic acid

Betulinic acid is a natural pentacyclic triterpenoid that displays anti-HIV and antitumor activity. Betulinic acid selectively induces apoptosis in tumor cells by directly activating the mitochondrial pathway of apoptosis through a p53- and CD95-independent mechanism. Betulinic acid also displays TGR5 agonist activity (EC50 =1.04 μM).

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References on Betulinic acid

[Research on HBV DNA inhibition of plasmid acute infection mouse with betulinic acid].[Pubmed:24956858]

Zhongguo Zhong Yao Za Zhi. 2014 Mar;39(6):1097-100.

Betulinic acid is a naturally occurring pentacyclic triterpenoid, which has antiretroviral, antimalarial, and anti-inflammatory properties. The purpose of this study is to investigate the HBV DNA replication inhibition in the mouse model with Betulinic acid. Hydrodynamic injection method via the tail vein with the Paywl. 3 plasmid was used to establish the animal mode (n = 15), and the mice were randomly divided into the PBS control group (n = 5), Betulinic acid treatment group (n = 5) and lamivudine control group (n = 5). The day after successful modeling , the mice would have taken Betulinic acid (100 mg x kg(-1)), lamivudine (50 mg x kg(-1)), PBS drugs orally, once daily for 7 days, blood samples were acquired from the orbital venous blood at 3, 5, 7 days after the administering, HBsAg and HBeAg in serum concentration were measured by ELISA and the mice were sacrificed after 7 days, HBV DNA southern detections were used with part of mice livers. The results showed that Betulinic acid significantly inhibited the expression of HbsAg in the mice model at the fifth day compared with the control group, and there was no significant differences between the effects of lamivudine and the PBS control group; both the Betulinic acid and lamivudine groups had no significant inhibition for the HBeAg expression; the HBV DNA expressions of the liver tissue from the Betulinic acid and lamivudine groups were inhibited compared with the control group. Taken together, these results reveal Betulinic acid can inhibit the HBsAg expression and replication of the liver HBV DNA in the mouse model.

Betulinic acid isolated from Vitis amurensis root inhibits 3-isobutyl-1-methylxanthine induced melanogenesis via the regulation of MEK/ERK and PI3K/Akt pathways in B16F10 cells.[Pubmed:24632067]

Food Chem Toxicol. 2014 Jun;68:38-43.

Previously, Betulinic acid was identified as one of the main compounds responsible for the anti-melanogenic effect in Vitis amurensis root. In this study, we investigated the precise mechanism underlying the anti-melanogenic activity of Betulinic acid in B16F10 cells. Betulinic acid significantly attenuated 3-isobutyl-1-methylxanthine (IBMX)-induced melanin production by inhibiting tyrosinase, tyrosinase related protein (TRP)-1, and TRP-2 expression through the modulation of their corresponding transcription factors, microphthalamia associated transcription factor (MITF) and cAMP response element binding protein (CREB), in B16F10 cells. In addition, phosphorylation of mitogen-activated protein kinase kinase (MEK)/extracellular regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/Akt, involved in the melanogenic processes, were ameliorated by Betulinic acid treatment. Role of MEK/ERK and PI3K/Akt signaling pathway in the melanogenesis was confirmed by using specific inhibitors, PD98059 (for MEK/ERK) and LY294002 (for PI3K/Akt), respectively. As a result, Betulinic acid inhibited melanin production by tyrosinase, TRP-1, and TRP-2 inhibition through the regulation of CREB and MITF, which was accompanied with MEK/ERK and PI3K/Akt inactivation in IBMX-stimulated B16F10 cells. Consequently, these results demonstrate a novel molecular function of Betulinic acid derived from V. amurensis root in melanogenesis, which in turn enhances our understanding on the application of cosmetic therapy for reducing skin hyperpigmentation.

Betulinic acid, a bioactive pentacyclic triterpenoid, inhibits skeletal-related events induced by breast cancer bone metastases and treatment.[Pubmed:24463094]

Toxicol Appl Pharmacol. 2014 Mar 1;275(2):152-62.

Many breast cancer patients experience bone metastases and suffer skeletal complications. The present study provides evidence on the protective and therapeutic potential of Betulinic acid on cancer-associated bone diseases. Betulinic acid is a naturally occurring triterpenoid with the beneficial activity to limit the progression and severity of cancer, diabetes, cardiovascular diseases, atherosclerosis, and obesity. We first investigated its effect on breast cancer cells, osteoblastic cells, and osteoclasts in the vicious cycle of osteolytic bone metastasis. Betulinic acid reduced cell viability and the production of parathyroid hormone-related protein (PTHrP), a major osteolytic factor, in MDA-MB-231 human metastatic breast cancer cells stimulated with or without tumor growth factor-beta. Betulinic acid blocked an increase in the receptor activator of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin ratio by downregulating RANKL protein expression in PTHrP-treated human osteoblastic cells. In addition, Betulinic acid inhibited RANKL-induced osteoclastogenesis in murine bone marrow macrophages and decreased the production of resorbed area in plates with a bone biomimetic synthetic surface by suppressing the secretion of matrix metalloproteinase (MMP)-2, MMP-9, and cathepsin K in RANKL-induced osteoclasts. Furthermore, oral administration of Betulinic acid inhibited bone loss in mice intra-tibially inoculated with breast cancer cells and in ovariectomized mice causing estrogen deprivation, as supported by the restored bone morphometric parameters and serum bone turnover markers. Taken together, these findings suggest that Betulinic acid may have the potential to prevent bone loss in patients with bone metastases and cancer treatment-induced estrogen deficiency.

Increase of betulinic acid production in Saccharomyces cerevisiae by balancing fatty acids and betulinic acid forming pathways.[Pubmed:24389702]

Appl Microbiol Biotechnol. 2014 Apr;98(7):3081-9.

Betulinic acid is a plant-based triterpenoid that has been recognized for its antitumor and anti-HIV activities. The level of Betulinic acid in its natural hosts is extremely low. In the present study, we constructed Betulinic acid biosynthetic pathway in Saccharomyces cerevisiae by metabolic engineering. Given the Betulinic acid forming pathways sharing the common substrate acetyl-CoA with fatty acid synthesis, the metabolic fluxes between the two pathways were varied by changing gene expressions, and their effects on Betulinic acid production were investigated. We constructed nine S. cerevisiae strains representing nine combinations of the flux distributions between Betulinic acid and fatty acid pathways. Our results demonstrated that it was possible to improve the Betulinic acid production in S. cerevisiae while keeping a desirable growth phenotype by optimally balancing the carbon fluxes of the two pathways. Through modulating the expressions of the key genes on Betulinic acid and fatty acid pathways, the difference in Betulinic acid yield varied largely in the range of 0.01-1.92 mg L(-1) OD(-1). The metabolic engineering approach used in this study could be extended for synthesizing other triterpenoids in S. cerevisiae.

Betulinic acid suppresses carcinogen-induced NF-kappa B activation through inhibition of I kappa B alpha kinase and p65 phosphorylation: abrogation of cyclooxygenase-2 and matrix metalloprotease-9.[Pubmed:12960358]

J Immunol. 2003 Sep 15;171(6):3278-86.

Betulinic acid (BA), a pentacyclic triterpene isolated from the bark of the white birch tree, has been reported to be a selective inducer of apoptosis in tumor cells. It also exhibits anti-inflammatory and immunomodulatory properties. How BA mediates these effects is not known. Because of the critical role of the transcription factor NF-kappaB in growth modulatory, inflammatory, and immune responses, we postulated that BA modulates the activity of this factor. In this study we investigated the effect of BA on NF-kappaB and NF-kappaB-regulated gene expression activated by a variety of inflammatory and carcinogenic agents. BA suppressed NF-kappaB activation induced by TNF, PMA, cigarette smoke, okadaic acid, IL-1, and H(2)O(2). The suppression of NF-kappaB activation was not cell-type specific. BA suppressed the activation of IkappaBalpha kinase, thus abrogating the phosphorylation and degradation of IkappaBalpha. We found that BA inhibited NF-kappaB activated by TNFR 1, TNFR-associated death domain, TNFR-associated factor 2, NF-kappaB-inducing kinase, and IkappaBalpha kinase. Treatment of cells with this triterpinoid also suppressed NF-kappaB-dependent reporter gene expression and the production of NF-kappaB-regulated gene products such as cyclooxygenase-2 and matrix metaloproteinase-9 induced by inflammatory stimuli. Furthermore, BA enhanced TNF-induced apoptosis. Overall, our results indicated that BA inhibits activation of NF-kappaB and NF-kappaB-regulated gene expression induced by carcinogens and inflammatory stimuli. This may provide a molecular basis for the ability of BA to mediate apoptosis, suppress inflammation, and modulate the immune response.

Structure-activity relationship study of betulinic acid, a novel and selective TGR5 agonist, and its synthetic derivatives: potential impact in diabetes.[Pubmed:19911773]

J Med Chem. 2010 Jan 14;53(1):178-90.

We describe here the biological screening of a collection of natural occurring triterpenoids against the G protein-coupled receptor TGR5, known to be activated by bile acids and which mediates some important cell functions. This work revealed that betulinic (1), oleanolic (2), and ursolic acid (3) exhibited TGR5 agonist activity in a selective manner compared to bile acids, which also activated FXR, the nuclear bile acid receptor. The most potent natural triterpenoid Betulinic acid was chosen as a reference compound for an SAR study. Hemisyntheses were performed on the Betulinic acid scaffold, and we focused on structural modifications of the C-3 alcohol, the C-17 carboxylic acid, and the C-20 alkene. In particular, structural variations around the C-3 position gave rise to major improvements of potency exemplified with derivatives 18 dia 2 (RG-239) and 19 dia 2. The best derivative was tested in vitro and in vivo, and its biological profile is discussed.

Betulinic Acid for cancer treatment and prevention.[Pubmed:19325847]

Int J Mol Sci. 2008 Jun;9(6):1096-107.

Betulinic acid is a natural product with a range of biological effects, for example potent antitumor activity. This anticancer property is linked to its ability to induce apoptotic cell death in cancer cells by triggering the mitochondrial pathway of apoptosis. In contrast to the cytotoxicity of Betulinic acid against a variety of cancer types, normal cells and tissue are relatively resistant to Betulinic acid, pointing to a therapeutic window. Compounds that exert a direct action on mitochondria present promising experimental cancer therapeutics, since they may trigger cell death under circumstances in which standard chemotherapeutics fail. Thus, mitochondrion-targeted agents such as Betulinic acid hold great promise as a novel therapeutic strategy in the treatment of human cancers.

Description

Betulinic acid is a natural pentacyclic triterpenoid, acts as a eukaryotic topoisomerase I inhibitor, with an IC50 of 5 μM, and possesses anti-HIV, anti-malarial, anti-inflammatory and anti-tumor properties. Betulinic acid acts as a new activator of NF-kB.

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