Cucurbitacin IIA

CAS# 58546-34-2

Cucurbitacin IIA

Catalog No. BCN5019----Order now to get a substantial discount!

Product Name & Size Price Stock
Cucurbitacin IIA: 5mg $92 In Stock
Cucurbitacin IIA: 10mg Please Inquire In Stock
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Quality Control of Cucurbitacin IIA

Number of papers citing our products

Chemical structure

Cucurbitacin IIA

3D structure

Chemical Properties of Cucurbitacin IIA

Cas No. 58546-34-2 SDF Download SDF
PubChem ID 181183 Appearance White powder
Formula C32H50O8 M.Wt 562.73
Type of Compound Triterpenoids Storage Desiccate at -20°C
Synonyms 25-Acetoxy 23,24-dihydrocucurbitacin F; 25-O-Acetyl 23,24-dihydrocucurbitacin F; Cucurbitacin IIa; Dihydrocucurbitacin F 25-O-acetate; Dihydrocucurbitacin Q1
Solubility Soluble in methan
Chemical Name [(6R)-6-hydroxy-2-methyl-5-oxo-6-[(2S,3S,8S,9R,10R,13R,14S,16R,17R)-2,3,16-trihydroxy-4,4,9,13,14-pentamethyl-11-oxo-1,2,3,7,8,10,12,15,16,17-decahydrocyclopenta[a]phenanthren-17-yl]heptan-2-yl] acetate
SMILES CC(=O)OC(C)(C)CCC(=O)C(C)(C1C(CC2(C1(CC(=O)C3(C2CC=C4C3CC(C(C4(C)C)O)O)C)C)C)O)O
Standard InChIKey LKYNAQSYQLFTCM-GYXNDICUSA-N
Standard InChI InChI=1S/C32H50O8/c1-17(33)40-27(2,3)13-12-23(36)32(9,39)25-21(35)15-29(6)22-11-10-18-19(14-20(34)26(38)28(18,4)5)31(22,8)24(37)16-30(25,29)7/h10,19-22,25-26,34-35,38-39H,11-16H2,1-9H3/t19-,20+,21-,22+,25+,26-,29+,30-,31+,32+/m1/s1
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 Cucurbitacin IIA

The rhizomes of Hemsleya amabilis Diels.

Biological Activity of Cucurbitacin IIA

DescriptionCucurbitacin IIa has anti-cancer, anti-bacterial, and anti-inflammatory effects, it can induce apoptosis and enhance autophagy; it also can disrupt the actin cytoskeleton and direct the cell to undergo PARP-mediated apoptosis through the inhibition of survivin downstream of JAK2/STAT3.
TargetsCaspase | NF-kB | TNF-α | PARP | JAK | STAT | MAPK
In vitro

Cucurbitacin IIa induces caspase-3-dependent apoptosis and enhances autophagy in lipopolysaccharide-stimulated RAW 264.7 macrophages.[Pubmed: 23541744]

Int Immunopharmacol. 2013 May;16(1):27-34.

Cucurbitacin IIA (CuIIa), a member of cucurbitacin family, is isolated from the root of Hemsleya amabilis which has been used as an ancient remedy for bacillary dysentery and gastroenteritis. The anti-inflammatory properties of Cucurbitacin IIA have long been recognized but the underlying mechanism is largely unknown.
METHODS AND RESULTS:
In this study, we investigated the anti-inflammatory effect of Cucurbitacin IIA on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. The results showed that Cucurbitacin IIA inhibited the proliferation and migration of RAW 264.7 cells in a dose-dependent manner. Whereas Cucurbitacin IIA did not cause apoptosis in unstimulated RAW 264.7 cells, it did induce a significant apoptosis in LPS-stimulated cells, which was caspase-3-dependent and associated with downregulation of survivin. Furthermore, LPS induced autophagy in RAW 264.7 cells and this effect was further enhanced by Cucurbitacin IIA as evidenced by increased levels of LC3-II conjugates and formation of LC3 puncta. In addition, Cucurbitacin IIA disrupted actin cytoskeleton via inducing actin aggregation. However, neither the synthesis of tumor necrosis factor-α, nor the activation of the mitogen-activated protein kinases and NF-κB pathways in LPS-stimulated cells was suppressed by Cucurbitacin IIA treatment.
CONCLUSIONS:
Collectively, these results suggested that induction of apoptosis and enhancement of autophagy contributed to the anti-inflammatory activity of Cucurbitacin IIA against inflammation-related diseases.

Protocol of Cucurbitacin IIA

Kinase Assay

Cucurbitacin IIa: a novel class of anti-cancer drug inducing non-reversible actin aggregation and inhibiting survivin independent of JAK2/STAT3 phosphorylation.[Pubmed: 21304528]

Br J Cancer. 2011 Mar 1;104(5):781-9.

Cucurbitacin (Cuc) and triterpene-derived natural products exhibit anti-cancer potential in addition to their conspicuous anti-bacterial and anti-inflammatory activity. Recently, inhibition of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling was shown to underlie the effects of Cuc family on inducing cell death in cancer.
METHODS AND RESULTS:
We purified Cucurbitacin IIA, the active component from the medicinal plant Hemsleya amalils Diels, which shows different structural modifications from other Cuc derivatives. We investigated the mechanisms of its inhibitory effects on cancer cells in vitro and tumour growth in vivo. Cucurbitacin IIA induced the irreversible clustering of filamentous actin and arrested cell cycle by the increases in G2/M populations. Cucurbitacin IIA resulted in the reduced phospho-Histone H3 and markedly increased cleavage of poly-(ADP-ribose) polymerase or PARP, immediate upstream of DNA breakdown as the result of caspase activation, consistent with mitotic blockage-induced cell death. However, unlike other Cuc members, Cucurbitacin IIA did not suppress JAK2/STAT3 phosphorylation or alter phosphorylation of mitogen-activated protein kinases. Instead, the expression of the cell cycle-regulated Inhibitor of Apoptosis Protein (IAP) survivin was reduced. Introducing oncoprotein δ-catenin, which increased survivin expression and suppressed small GTPase RhoA, reduced efficacy of Cucurbitacin IIA to induce cell death. Supporting the effects of Cucurbitacin IIA on actin cytoskeletal signaling, RhoA phosphorylation was reduced suggesting its increased activity.
CONCLUSIONS:
Cucurbitacin IIA is a novel class of anti-cancer drug in suppression of cancer cell expansion by disrupting the actin cytoskeleton and directing the cell to undergo PARP-mediated apoptosis through the inhibition of survivin downstream of JAK2/STAT3.

Cucurbitacin IIA Dilution Calculator

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Cucurbitacin IIA Molarity Calculator

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Preparing Stock Solutions of Cucurbitacin IIA

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.7771 mL 8.8853 mL 17.7705 mL 35.541 mL 44.4263 mL
5 mM 0.3554 mL 1.7771 mL 3.5541 mL 7.1082 mL 8.8853 mL
10 mM 0.1777 mL 0.8885 mL 1.7771 mL 3.5541 mL 4.4426 mL
50 mM 0.0355 mL 0.1777 mL 0.3554 mL 0.7108 mL 0.8885 mL
100 mM 0.0178 mL 0.0889 mL 0.1777 mL 0.3554 mL 0.4443 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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References on Cucurbitacin IIA

Cucurbitacin IIa: a novel class of anti-cancer drug inducing non-reversible actin aggregation and inhibiting survivin independent of JAK2/STAT3 phosphorylation.[Pubmed:21304528]

Br J Cancer. 2011 Mar 1;104(5):781-9.

BACKGROUND: Cucurbitacin (Cuc) and triterpene-derived natural products exhibit anti-cancer potential in addition to their conspicuous anti-bacterial and anti-inflammatory activity. Recently, inhibition of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling was shown to underlie the effects of Cuc family on inducing cell death in cancer. METHOD: We purified Cuc IIa, the active component from the medicinal plant Hemsleya amalils Diels, which shows different structural modifications from other Cuc derivatives. We investigated the mechanisms of its inhibitory effects on cancer cells in vitro and tumour growth in vivo. RESULTS: Cuc IIa induced the irreversible clustering of filamentous actin and arrested cell cycle by the increases in G2/M populations. Cuc IIa resulted in the reduced phospho-Histone H3 and markedly increased cleavage of poly-(ADP-ribose) polymerase or PARP, immediate upstream of DNA breakdown as the result of caspase activation, consistent with mitotic blockage-induced cell death. However, unlike other Cuc members, Cuc IIa did not suppress JAK2/STAT3 phosphorylation or alter phosphorylation of mitogen-activated protein kinases. Instead, the expression of the cell cycle-regulated Inhibitor of Apoptosis Protein (IAP) survivin was reduced. Introducing oncoprotein delta-catenin, which increased survivin expression and suppressed small GTPase RhoA, reduced efficacy of Cuc IIa to induce cell death. Supporting the effects of Cuc IIa on actin cytoskeletal signaling, RhoA phosphorylation was reduced suggesting its increased activity. CONCLUSION: Cuc IIa is a novel class of anti-cancer drug in suppression of cancer cell expansion by disrupting the actin cytoskeleton and directing the cell to undergo PARP-mediated apoptosis through the inhibition of survivin downstream of JAK2/STAT3.

Cucurbitacin IIa induces caspase-3-dependent apoptosis and enhances autophagy in lipopolysaccharide-stimulated RAW 264.7 macrophages.[Pubmed:23541744]

Int Immunopharmacol. 2013 May;16(1):27-34.

Cucurbitacin IIA (CuIIa), a member of cucurbitacin family, is isolated from the root of Hemsleya amabilis which has been used as an ancient remedy for bacillary dysentery and gastroenteritis. The anti-inflammatory properties of CuIIa have long been recognized but the underlying mechanism is largely unknown. In this study, we investigated the anti-inflammatory effect of CuIIa on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. The results showed that CuIIa inhibited the proliferation and migration of RAW 264.7 cells in a dose-dependent manner. Whereas CuIIa did not cause apoptosis in unstimulated RAW 264.7 cells, it did induce a significant apoptosis in LPS-stimulated cells, which was caspase-3-dependent and associated with downregulation of survivin. Furthermore, LPS induced autophagy in RAW 264.7 cells and this effect was further enhanced by CuIIa as evidenced by increased levels of LC3-II conjugates and formation of LC3 puncta. In addition, CuIIa disrupted actin cytoskeleton via inducing actin aggregation. However, neither the synthesis of tumor necrosis factor-alpha, nor the activation of the mitogen-activated protein kinases and NF-kappaB pathways in LPS-stimulated cells was suppressed by CuIIa treatment. Collectively, these results suggested that induction of apoptosis and enhancement of autophagy contributed to the anti-inflammatory activity of CuIIa against inflammation-related diseases.

Description

Cucurbitacin IIa is a triterpene isolated from Hemsleya amalils Diels, induces apoptosis of cancer cells, reduces expression of survivin, reduces phospho-Histone H3 and increases cleaved PARP in cancer cells.

Keywords:

Cucurbitacin IIA,58546-34-2,25-Acetoxy 23,24-dihydrocucurbitacin F; 25-O-Acetyl 23,24-dihydrocucurbitacin F; Cucurbitacin IIa; Dihydrocucurbitacin F 25-O-acetate; Dihydrocucurbitacin Q1,Natural Products, buy Cucurbitacin IIA , Cucurbitacin IIA supplier , purchase Cucurbitacin IIA , Cucurbitacin IIA cost , Cucurbitacin IIA manufacturer , order Cucurbitacin IIA , high purity Cucurbitacin IIA

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