Vitexicarpin (Casticin)是一种含有三个苯环的非同位素四甲氧基黄酮，是一种具有高细胞毒性的磷脂酰肌醇3-激酶(PI3K)抑制剂。
Cas No.:479-91-4
Sample solution is provided at 25 µL, 10mM.
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Vitexicarpin (Casticin), a non-isotopic tetramethoxyflavone with three phenyl rings, is a phosphatidylinositol 3-kinase (PI3K) inhibitor with high cytotoxicity [1]. Vitexicarpin can down-regulate the mRNA and protein levels of DNA methyltransferase 1(DNMT1) and induce DNA damage by binding to topoisomerase IIα[2]. Vitexicarpin has been widely used as an anticancer agent to inhibit the malignant progression of cancer cells in diverse tumor cell models[3].
In vitro, Vitexicarpin significantly inhibited the proliferation of K562, HL-60, and Kasumi-1 cells with IC50 values of 5.95μM, 4.82μM, and 15.56μM, respectively[4]. Treatment with Vitexicarpin at 8µM for 24h significantly induced apoptosis and G2/M phase arrest in S18 cells[5]. Treatment of MGC803 cells with 30µM Vitexicarpin for 72h significantly reduced cell viability, increased protein expression and mRNA levels of RECK, and decreased global DNA methylation levels[6].
In vivo, Vitexicarpin treatment (20mg/kg/day) via intragastric administration for 2 weeks significantly reduced liver injury and liver fibrosis induced by bile duct ligation in mice[7]. Vitexicarpin(0.4mg/kg) was injected intraperitoneally once every two days for 18 days, which significantly reduced the tumor volume and weight of SCC-4 cell xenograft mice without affecting the body weight of the mice[8].
References:
[1] Ramchandani S, Naz I, Lee J H, et al. An overview of the potential antineoplastic effects of casticin[J]. Molecules, 2020, 25(6): 1287.
[2] Carbone K, Gervasi F, Kozhamzharova L, et al. Casticin as potential anticancer agent: recent advancements in multi-mechanistic approaches[J]. Frontiers in Molecular Biosciences, 2023, 10: 1157558.
[3] Ding X J, Cai X M, Wang Q Q, et al. Vitexicarpin suppresses malignant progression of colorectal cancer through affecting c-Myc ubiquitination by targeting IMPDH2[J]. Phytomedicine, 2024, 132: 155833.
[4] Shen J K, Du H, Yang M, et al. Casticin induces leukemic cell death through apoptosis and mitotic catastrophe[J]. Annals of hematology, 2009, 88(8): 743-752.
[5] Liu J, Yang J, Hou Y, et al. Casticin inhibits nasopharyngeal carcinoma growth by targeting phosphoinositide 3-kinase[J]. Cancer cell international, 2019, 19(1): 348.
[6] Yang F, He K, Huang L, et al. Casticin inhibits the activity of transcription factor Sp1 and the methylation of RECK in MGC803 gastric cancer cells[J]. Experimental and Therapeutic Medicine, 2017, 13(2): 745-750.
[7] Zhou L, Dong X, Wang L, et al. Casticin attenuates liver fibrosis and hepatic stellate cell activation by blocking TGF-β/Smad signaling pathway[J]. Oncotarget, 2017, 8(34): 56267.
[8] Shang H S, Chen K W, Chou J S, et al. Casticin inhibits in vivo growth of xenograft tumors of human oral cancer SCC-4 cells[J]. in vivo, 2020, 34(5): 2461-2467.
Vitexicarpin (Casticin)是一种含有三个苯环的非同位素四甲氧基黄酮，是一种具有高细胞毒性的磷脂酰肌醇3-激酶(PI3K)抑制剂[1]。Vitexicarpin能够下调DNA甲基转移酶1的mRNA和蛋白水平，并通过与拓扑异构酶IIα结合诱导DNA损伤[2]。Vitexicarpin已被广泛用作抗癌剂，在多种肿瘤细胞模型中抑制癌细胞的恶性进展[3]。
在体外，Vitexicarpin显著抑制K562、HL-60和Kasumi-1细胞的增殖，IC50值分别为5.95μM、4.82μM和15.56μM[4]。用8µM的Vitexicarpin处理S18细胞24小时，能显著诱导细胞凋亡和G2/M期阻滞[5]。用30µM的Vitexicarpin处理MGC803细胞72小时，显著降低了细胞活力，增加了RECK的蛋白表达和mRNA水平，并降低了整体DNA甲基化水平[6]。
在体内，通过灌胃给予Vitexicarpin（20mg/kg/day）治疗2周，显著减轻了小鼠胆管结扎诱导的肝损伤和肝纤维化[7]。每两天腹腔注射一次Vitexicarpin（0.4mg/kg），持续18天，显著降低了SCC-4细胞异种移植小鼠的肿瘤体积和重量，且不影响小鼠体重 [8]。
| Cell experiment [1]: | |
Cell lines | A549 cells |
Preparation Method | A549 cells were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FCS), 100U/ml penicillin, and 100μg/ml streptomycin in a humidified incubator at 37°C and 5% CO2. Cells were seeded in 96-well plates at a density of 5×103 cells/well at 100μl per well and treated with different concentrations of Vitexicarpin (0, 10, 20, 30, 40, and 50μM). After 24, 48, and 72 hours of incubation, 10μl of CCK-8 reagent was added to each well, and incubation was continued for 1 or 2 hours. Then, the absorbance value at 490nm was measured for each well. |
Reaction Conditions | 0, 10, 20, 30, 40, and 50μM; 24, 48, and 72h |
Applications | Vitexicarpin treatment inhibited the proliferation of A549 cells in a concentration- and time-dependent manner. |
| Animal experiment [2]: | |
Animal models | BALB/c nude mice |
Preparation Method | Five-week-old BALB/c nude mice were maintained in a standard environment with ad libitum access to diet and water. 5×106 S18 cells were subcutaneously injected into the left side of the back of each mouse (3 mice per group). When the tumor volume reached approximately 100mm3, mice were randomly divided into control and vitexin treatment groups. Vitexicarpin was diluted in 10% DMSO in normal saline, and Vitexicarpin was injected intraperitoneally at a dose of 40mg/kg daily for 18 days; the control group was injected with normal saline only. Tumor size was measured and recorded every 3 days using a vernier caliper. |
Dosage form | 40mg/kg/day for 18 days; i.p. |
Applications | Vitexicarpin treatment significantly reduced tumor growth in the S18 cell-xenograft mouse models. |
References: | |
| Cas No. | 479-91-4 | SDF | |
| 别名 | 蔓荆子黄素; Vitexicarpin | ||
| 化学名 | 5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-3,6,7-trimethoxychromen-4-one | ||
| Canonical SMILES | COC1=C(C=C(C=C1)C2=C(C(=O)C3=C(C(=C(C=C3O2)OC)OC)O)OC)O | ||
| 分子式 | C19H18O8 | 分子量 | 374.35 |
| 溶解度 | ≥ 37.4mg/mL in DMSO | 储存条件 | 4°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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.6713 mL | 13.3565 mL | 26.713 mL |
| 5 mM | 534.3 μL | 2.6713 mL | 5.3426 mL |
| 10 mM | 267.1 μL | 1.3356 mL | 2.6713 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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