Kaurenoic acid
(Synonyms: 异贝壳杉烯酸；贝壳杉烯酸) 目录号 : GC36387
A diterpene with diverse biological activities
Cas No.:6730-83-2
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
Kaurenoic acid is a diterpene that has been found in C. langsdorffii and has diverse biological activities, including anticancer, antibacterial, antioxidant, and anti-inflammatory properties.1,2,3 It is cytotoxic to 22Rv1 and LNCaP prostate, HT-29, HCT116, SW480, and SW620 colon, and MCF-7 breast cancer cells with IC50 values ranging from 15.03 to 48.87 μg/ml.2 Kaurenoic acid is active against S. epidermidis, S. capitis, E. faecalis, and S. haemolyticus in vitro (MICs = 6.25-12.5 μg/ml).3 Kaurenoic acid (50 and 100 mg/kg) reduces colonic myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels in a rat model of acetic acid-induced colitis, as well as colonic tissue damage, leukocytic infiltration, and submucosal edema when administered at a dose of 100 mg/kg.1
1.Paiva, L.A.F., Gurgel, L.A., Silva, R.M., et al.Anti-inflammatory effect of kaurenoic acid, a diterpene from Copaifera langsdorffi on acetic acid-induced colitis in ratsVascul. Pharmacol.39(6)303-307(2003) 2.Henry, G.E., Adams, L.S., Rosales, J.C., et al.Kaurene diterpenes from Laetia thamnia inhibit the growth of human cancer cells in vitroCancer Lett.244(2)190-194(2006) 3.Soares, A.C.F., Matos, P.M., Dias, H.J., et al.Variability of the antibacterial potential among analogue diterpenes against Gram-positive bacteria: Considerations on structure-activity subjectCan. J. Chem.97(7)568-575(2019)
| Cas No. | 6730-83-2 | SDF | |
| 别名 | 异贝壳杉烯酸；贝壳杉烯酸 | ||
| Canonical SMILES | C[C@@]1(C(O)=O)CCC[C@@]2(C)[C@@]3([H])[C@@]4(CC([C@H](CC3)C4)=C)CC[C@]12[H] | ||
| 分子式 | C20H30O2 | 分子量 | 302.45 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 25 mg/ml,DMSO:PBS (pH 7.2) (1:2): 0.3 mg/ml,Ethanol: 10 mg/ml | 储存条件 | -20°C, protect from light |
| 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 | 3.3063 mL | 16.5317 mL | 33.0633 mL |
| 5 mM | 0.6613 mL | 3.3063 mL | 6.6127 mL |
| 10 mM | 0.3306 mL | 1.6532 mL | 3.3063 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。
Kaurenoic acid activates TGF-β signaling
Phytomedicine 2017 Aug 15;32:8-14.PMID:28732811DOI:10.1016/j.phymed.2017.04.008.
Background: Kaurenoic acid (ent-kaur-16-en-19-oic acid: KA) is a key constituent found in the roots of Aralia continentalis Kitagawa (Araliaceae) that has been used for treating rheumatism in traditional Asian medicine. Hypothesis: Although KA was reported to suppress inflammation by activating Nrf2, the anti-inflammatory function of KA is less characterized. Given the complex nature of the inflammatory response and the critical role of TGF-β in resolving inflammation, we hypothesized that KA suppresses inflammatory response by activating TGF-β signaling. Methods: Murine macrophage RAW 264.7, human lung epithelial cell MRC-5, and a TGFβRII defective cell HCT116 were treated with various amounts of KA. KA was also administered to mouse lung via intratracheal (i.t.) route. Phosphorylated Smad2 and Smad3 were analyzed by western blot. TGFβ-dependent gene expression was determined by immunoblotting of α-SMA and luciferase assay. Results: KA induced the phosphorylation of Smad2 and Smad3, key activator molecules in TGF-β signaling. EW7197, an inhibitor for activin receptor-like kinase 5/TGF-β receptor I (TGFβR1) suppressed KA-mediated phosphorylation of Smad2. Similarly, KA failed to phosphorylate Smad2 in HCT116, suggesting that KA acts through the prototypic TGFβR. KA treatment increased the transcriptional activity driven by a Smad-binding element in a luciferase reporter assay and induced the α-smooth muscle actin (α-SMA). Similarly, i.t. KA induced the phosphorylation of Smad2 and increased the expression ofα-SMA in mouse lungs. Conclusion: KA activated TGF-β signaling, suggesting that TGFβ signaling is associated with KA suppressing inflammation.
Kaurenoic acid nanocarriers regulates cytokine production and inhibit breast cancer cell migration
J Control Release 2022 Dec;352:712-725.PMID:36374787DOI:10.1016/j.jconrel.2022.10.048.
Breast cancer is the type of cancer with the highest incidence in women around the world. Noteworthy, the triple-negative subtype affects 20% of the patients while presenting the highest death rate among subtypes. This is due to its aggressive phenotype and the capability of invading other tissues. In general, tumor-associated macrophages (TAM) and other immune cells, are responsible for maintaining a favorable tumor microenvironment for inflammation and metastasis by secreting several mediators such as pro-inflammatory cytokines IL-1β, IL-6, and TNF-α, chemokines like CCL2, and other proteins, as metalloproteinases of matrix (MMP). On the other hand, immunomodulatory agents can interfere in the immune response of TAM and change the disease prognosis. In this work, we prepared nanostructured lipid carriers containing Kaurenoic acid (NLC-KA) to evaluate the effect on cytokine production in vitro of bone marrow-derived macrophages (BMDM) and the migratory process of 4 T1 breast cancer cells. NLC-KA prepared from a blend of natural lipids was shown to have approximately 90 nm in diameter with low polydispersity index. To test the effect on cytokine production in vitro in NLC-KA treated BMDM, ELISA assay was performed and pro-inflammatory cytokines IL-1β, IL-6, and TNF-α were quantified. The formulation reduced the secretion of IL-1β and TNF-α cytokines while presenting no hemolytic activity. Noteworthy, an anti-migratory effect in 4 T1 breast cancer cells treated with NLC-KA was observed in scratch assays. Further, MMP9 and CCL2 gene expressions in both BMDM and 4 T1 treated cells confirmed that the mechanism of inhibition of migration is related to the blockade of this pathway by KA. Finally, cell invasion assays confirmed that NLC-KA treatment resulted in less invasiveness of 4 T1 cells than control, and it is independent of CCL2 stimulus or BMDM direct stimulus. Ultimately, NLC-KA was able to regulate the cytokine production in vitro and reduce the migration of 4 T1 breast cancer cells by decreasing MMP9 gene expression.
Continentalic Acid Rather Than Kaurenoic acid Is Responsible for the Anti-Arthritic Activity of Manchurian Spikenard In Vitro and In Vivo
Int J Mol Sci 2019 Nov 4;20(21):5488.PMID:31690022DOI:10.3390/ijms20215488.
The aim of this study was to identify the active compound responsible for the pharmacological activities of Manchurian spikenard (Aralia continentalis Kitag.). Interleukin (IL)-1β-stimulated human chondrocytes and monoiodoacetate (MIA)-induced osteoarthritic rats were treated with the 50% ethanolic extract of spikenard or its major components, such as continentalic acid (ent-pimara-8(14),15-diene-19-oic acid) and Kaurenoic acid (ent-kaura-16-en-19-oic acid). The spikenard extract significantly inhibited IL-1β-stimulated production of IL-6, IL-8, metalloproteinase (MMP)-1, MMP-13, cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) and prostaglandin(PG)E2 in a dose-dependent manner but not MMP-3 production. The extract also inhibited the IL-1β-induced translocation of NF-κB/p65 into the nucleus and dose-dependent phosphorylation levels of extracellular signal-regulated kinase (ERK), Jun amino-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase. Continentalic acid exhibited significant anti-arthritic activity corresponding exactly to that of the extract containing an equivalent amount of continentalic acid. On the other hand, Kaurenoic acid exhibited a compatible activity at about a 10-times higher molar concentration than that of continentalic acid. In vitro anti-arthritic activities of the spikenard extract and continentalic acid were also confirmed in MIA-induced osteoarthritic rats. The 50% ethanolic extract of Manchurian spikenard exhibited promising anti-arthritic activities in the in vitro and in vivo osteoarthritis models, and continentalic acid, not Kaurenoic acid, was most probably responsible for those activities.
Determination of Kaurenoic acid in rat plasma using UPLC-MS/MS and its application to a pharmacokinetic study
J Pharm Biomed Anal 2019 Feb 5;164:27-31.PMID:30339948DOI:10.1016/j.jpba.2018.10.016.
Kaurenoic acid (KA), a kaurane diterpene found in several medicinal plants, is an active ingredient with potential anti-inflammatory, anticonvulsant, antibacterial and antitumor activities. In this work, an ultra-performance liquid chromatography-tandem mass spectrometry method (UPLC-MS/MS) was firstly developed and validated to quantify Kaurenoic acid in rat plasma. Rhein was chosen as the internal standard (IS) and the plasma was processed with one-step acetonitrile protein precipitation; the chromatographic separation was achieved on a HSS T3 (2.1 × 50 mm, 1.8 μm) column with the mobile phase consisting of acetonitrile and water containing 0.1% formic acid via gradient elution. An electrospray ionization source was applied and operated in the negative ion and multiple reaction monitoring (MRM) modes. Kaurenoic acid and IS were quantified using the transitions of m/z 301.2→301.2 (pseudo MRM) and m/z 283.2 → 238.9, respectively. The calibration curves were linear over the range of 5∼ 100 ng/mL (R2 = 0.990). The lower limit of quantification (LLOQ) was 5 ng/mL. The intra- and inter- day precision (RSD) ranged from 3.0% to 11.4%. The matrix effect and extraction recovery were within acceptable limits. The validated method was successfully applied to the pharmacokinetic study of Kaurenoic acid in rats after oral administration at three dosages.
Kaurenoic acid Possesses Leishmanicidal Activity by Triggering a NLRP12/IL-1β/cNOS/NO Pathway
Mediators Inflamm 2015;2015:392918.PMID:26074677DOI:10.1155/2015/392918.
Leishmania amazonensis (L. amazonensis) infection can cause severe local and diffuse injuries in humans, a condition clinically known as American cutaneous leishmaniasis (ACL). Currently, the therapeutic approach for ACL is based on Glucantime, which shows high toxicity and poor effectiveness. Therefore, ACL remains a neglected disease with limited options for treatment. Herein, the in vitro antiprotozoal effect and mechanisms of the diterpene Kaurenoic acid [ent-kaur-16-en-19-oic acid] (KA) against L. amazonensis were investigated. KA exhibited a direct antileishmanial effect on L. amazonensis promastigotes. Importantly, KA also reduced the intracellular number of amastigote forms and percentage of infected peritoneal macrophages of BALB/c mice. Mechanistically, KA treatment reestablished the production of nitric oxide (NO) in a constitutive NO synthase- (cNOS-) dependent manner, subverting the NO-depleting escape mechanism of L. amazonensis. Furthermore, KA induced increased production of IL-1β and expression of the inflammasome-activating component NLRP12. These findings demonstrate the leishmanicidal capability of KA against L. amazonensis in macrophage culture by triggering a NLRP12/IL-1β/cNOS/NO mechanism.