RH1 (NSC 697726) is a potent bioreductive agent with profound anti-cancer activity in vitro and in vivo.
体外研究 (In Vitro)
Treatment of NQ16 cells with RH1 (50 and 100 nM) for 60 and 120 min results in a significant increase (p< 0.05) in cross-linked DNA. RH1 induces apoptosis in a time- and concentration-dependent manner in NQ16 cells [1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
RH1 exhibits antitumor activity in a dose-dependent manner against NQ16 tumors growing in athymic mice. RH1 treatment (0.4 mg/kg and 0.2 mg/kg) of mice bearing NQ16 tumors results in a significant reduction in tumor volume between treated groups and controls as early as 5 days after the treatment period ended. Low-dose RH1 (0.1 mg/kg) also results in a significant reduction in tumor volume between treated mice and controls[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
234.25
Formula
C12H14N2O3
CAS 号
221635-42-3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Park MT, et al. The anti-tumour compound, RH1, causes mitochondria-mediated apoptosis by activating c-Jun N-terminal kinase. Br J Pharmacol. 2011 Jun;163(3):567-85.
[2]. Dehn DL, et al. Development of a new isogenic cell-xenograft system for evaluation of NAD(P)H:quinone oxidoreductase-directed antitumor quinones: evaluation of the activity of RH1. Clin Cancer Res. 2004 May 1;10(9):3147-55.
Cell Assay [1]
MDA468 and NQ16 cells are treated with RH1 at 50, 100, and 500 nM or 10, 50, and 100 nM, respectively, in unsupplemented media for 30, 60, or 120 min, after which the dosing medium is aspirated, rinsed with PBS, and then harvested[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice[2]
Female athymic nude mice bearing bilateral tumors are randomized into a control and three drug-treatment groups of seven to eight animals per cell line. RH1 (0.1 mg/kg, 0.2 mg/kg, or 0.4 mg/kg) is injected into mice daily for five consecutive days (every day for 5 days)[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Park MT, et al. The anti-tumour compound, RH1, causes mitochondria-mediated apoptosis by activating c-Jun N-terminal kinase. Br J Pharmacol. 2011 Jun;163(3):567-85.
[2]. Dehn DL, et al. Development of a new isogenic cell-xenograft system for evaluation of NAD(P)H:quinone oxidoreductase-directed antitumor quinones: evaluation of the activity of RH1. Clin Cancer Res. 2004 May 1;10(9):3147-55.
Highly active LHRH agonist that stimulates the pituitary release of luteinizing hormone and increases testicular androgen, therefore serving as a safer alternative to estrogens.
溶解度
分子量
1339.5
化学式
C66H86N18O13
存储条件
Store at -20°C. Keep tightly closed. Store in a cool dry place.
Ginsenoside Rh2 induces the activation of caspase-8 and caspase-9. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner.
IC50 & Target[1]
Caspase-8
Caspase-9
Apoptosis
Human Endogenous Metabolite
体外研究 (In Vitro)
Ginsenoside Rh2 induces the activation of two initiator caspases, caspase-8 and caspase-9 in human cancer cells. Ginsenoside Rh2 induces cancer cell apoptosis in a multi-path manner and is therefore a promising candidate for anti-tumor drug development. Ginsenoside Rh2 triggers p53-dependent Fas expression and consequent activation of caspase-8 and p53-independent caspase-9-mediated intrinsic pathway to cause cancer cell death.The cytotoxic activity of Ginsenoside Rh2 in the human tumor cell lines HeLa, SK-HEP-1, SW480, and PC-3 is assessed by MTT. The cell viability of HeLa cells is remarkably inhibited by Ginsenoside Rh2, with an IC50 value of 2.52 μg/mL, whereas SK-HEP-1 and SW480 cells are less sensitive to Ginsenoside Rh2, with IC50 values of 3.15 μg/mL and 4.06 μg/mL, respectively. PC-3 cells are the least vulnerable to Ginsenoside Rh2, with an IC50 value of 7.85 μg/mL, 3-fold higher than HeLa cells[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
A total of 15 days following B16-F10 cell injection, tumor sizes from the 3 tumor bearing groups are measured. The tumor sizes in the G-L group and G-H group (G-L and G-H refer to a low or high dose of ginsenoside Rh2 injection) are reduced compared with the tumor group (P<0.05). The survival analysis reveals that the Ginsenoside Rh2 treated groups survive longer than the untreated tumor group and the effect is dose-dependent (P<0.05)[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
622.87
Formula
C36H62O8
CAS 号
78214-33-2
中文名称
人参皂苷 Rh2;人参皂苷 Rh2
运输条件
Room temperature in continental US; may vary elsewhere.
将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中,再用生理盐水定容至 10 mL,完全溶解,澄清透明
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Guo XX, et al. p53-dependent Fas expression is critical for Ginsenoside Rh2 triggered caspase-8 activation in HeLa cells. Protein Cell. 2014 Mar;5(3):224-34.
[2]. Wang M, et al. Ginsenoside Rh2 enhances the antitumor immunological response of a melanoma mice model. Oncol Lett. 2017 Feb;13(2):681-685.
Kinase Assay [1]
HeLa, SK-HEP-1, SW480, and PC-3 cells are treated with Ginsenoside Rh2 (7.5 μg/mL) in serum free media for indicated time periods and then are harvested. Fifty micrograms of cell lysates are incubated with 200 nM Ac-DEVD-AFC (for caspase-3), Ac-IETD-AFC (for caspase-8), and Ac-LEHD-AFC (for caspase-9) in a reaction buffer containing 20 mM HEPES, pH 7.4, 100 mM NaCl, 10 mM DTT, 0.1% CHAPS, and 10% sucrose at 37°C for 1 h. The reaction is monitored by fluorescence emission at 535 nm and excitation at 405 nm[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
Determination of cell viability is performed by using MTT assay, which is used to calculate the growth inhibition induced by increasing concentrations of drug. Briefly, exponentially growing HeLa, SK-HEP-1, SW480, and PC-3 cells are seeded into a 96-well plate at 1×104 cells/well in triplicate. After incubation for 24 h, cells are treated with increasing concentration of Ginsenoside Rh2 (1, 2.5, 5, 7.5 and 10 μg/mL) in serum free media for 48 h. At the end of treatment, 20 μL of MTT (5 mg/mL) is added to each well and incubated for an additional 4 h. The formazan grains formed by viable cells are solubilized with DMSO, and the color intensity is measured at 550 nm with an ELISA reader[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice[2] Male C57BL6 mice (3-4 weeks old) are randomly arranged into 4 groups of 80 mice: Tumor group, G-L group, G-H group and Control group. G-L and G-H refer to a low or high dose of ginsenoside Rh2 injection. For the tumor group, G-L group and G-H group, the B16-F10 cell line is injected into the mice. These 3 groups become tumor bearing groups. For the control group, the same volume of PBS is injected instead. Ginsenoside Rh2 is injected into the left back of mice in the G-L and G-H groups. The dose for the G-H group is 0.5 mg/kg or 0.2 mg/kg for G-L group, every 2 days after day 5. PBS is injected in the tumor and control groups at the same time points.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Guo XX, et al. p53-dependent Fas expression is critical for Ginsenoside Rh2 triggered caspase-8 activation in HeLa cells. Protein Cell. 2014 Mar;5(3):224-34.
[2]. Wang M, et al. Ginsenoside Rh2 enhances the antitumor immunological response of a melanoma mice model. Oncol Lett. 2017 Feb;13(2):681-685.
Mutant IDH1-IN-1 is a mutant-selective IDH1 inhibitor with with IC50s of 4, 42, 80 and 143 nM against mutant IDH1 R132C/R132C, IDH1 R132H/R132H, IDH1 R132H/WT and wild type IDH1, respectively.
[1]. Deng G, et al. Selective inhibition of mutant isocitrate dehydrogenase 1 (IDH1) via disruption of a metal binding network by an allosteric small molecule. J Biol Chem. 2015 Jan 9;290(2):762-74.