Cat. No.: HY-N21664

Schisanlactone B

Schisanlactone B is a glutathione S-transferase (GST) inhibitor with an IC₅₀ of 5 μM. Schisanlactone B binds to GST and inhibits its enzymatic activity. Schisanlactone B induces apoptosis and cell cycle arrest. Schisanlactone B can be used in research related to various cancers such as hepatocellular carcinoma, leukemia, melanoma, lung cancer, gastric cancer, and breast cancer.

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CAS No.: 87164-32-7
화학식: C₃₀H₄₂O₄
분자량:466.66

보관:

Please store the product under the recommended conditions in the Certificate of Analysis.

Schisanlactone B Chemical Structure

CAS No.: 87164-32-7

Amount: USD 0.00

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- 제품 설명
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
순도&문서
References
Calculators
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

IC₅₀ & Target

^[1]

GST

5 μM (IC₅₀)

Cellular Effect

Cell Line	Type	Value	Description	References
HL-60	IC50	34.72 μM	Cytotoxicity against human HL-60 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human HL-60 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	16557460
Bel-7402	IC50	100 μM	Cytotoxicity against human Bel-7402 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay. Cytotoxicity against human Bel-7402 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.	16557460
CCRF-CEM	IC50	4.66 μg/mL	Cytotoxic activity against murine leukemia CCRF-CEM cells assessed as reduction in cell viability incubated for 24 hrs by crystal violet protein staining method. Cytotoxic activity against murine leukemia CCRF-CEM cells assessed as reduction in cell viability incubated for 24 hrs by crystal violet protein staining method.	14661856
HeLa	IC50	46.6 μg/mL	Cytotoxic activity against human Hela cells assessed as reduction in cell viability incubated for 24 hrs by crystal violet protein staining method. Cytotoxic activity against human Hela cells assessed as reduction in cell viability incubated for 24 hrs by crystal violet protein staining method.	14661856
NCI-H23	GI50	1.28 μM	Antiproliferative activity against human NCI-H23 lung cancer cells assessed as reduction in cell growth by SRB assay. Antiproliferative activity against human NCI-H23 lung cancer cells assessed as reduction in cell growth by SRB assay.	34075849
NUGC-3	GI50	1.80 μM	Antiproliferative activity against human NUGC-3 stomach cancer cells assessed as reduction in cell growth by SRB assay. Antiproliferative activity against human NUGC-3 stomach cancer cells assessed as reduction in cell growth by SRB assay.	34075849
PC-3	GI50	2.33 μM	Antiproliferative activity against human PC-3 prostate cancer cells assessed as reduction in cell growth by SRB assay. Antiproliferative activity against human PC-3 prostate cancer cells assessed as reduction in cell growth by SRB assay.	34075849
MDA-MB-231	GI50	2.38 μM	Antiproliferative activity against human MDA-MB-231 breast cancer cells assessed as reduction in cell growth by SRB assay. Antiproliferative activity against human MDA-MB-231 breast cancer cells assessed as reduction in cell growth by SRB assay.	34075849
ACHN	GI50	2.63 μM	Antiproliferative activity against human ACHN renal cancer cells assessed as reduction in cell growth by SRB assay. Antiproliferative activity against human ACHN renal cancer cells assessed as reduction in cell growth by SRB assay.	34075849
HCT-15	GI50	2.67 μM	Antiproliferative activity against human HCT-15 colon cancer cells assessed as reduction in cell growth by SRB assay. Antiproliferative activity against human HCT-15 colon cancer cells assessed as reduction in cell growth by SRB assay.	34075849
A549	GI50	17.47 μM	Cytotoxicity against human lung carcinoma A549 cells assessed as growth inhibition incubated for 72 hrs by sulforhodamine B colorimetric assay. Cytotoxicity against human lung carcinoma A549 cells assessed as growth inhibition incubated for 72 hrs by sulforhodamine B colorimetric assay.	23883077
PC-3	GI50	18.09 μM	Cytotoxicity against human prostate carcinoma PC-3 cells assessed as growth inhibition incubated for 72 hrs by sulforhodamine B colorimetric assay. Cytotoxicity against human prostate carcinoma PC-3 cells assessed as growth inhibition incubated for 72 hrs by sulforhodamine B colorimetric assay.	23883077
KB	GI50	15.02 μM	Cytotoxicity against human epidermoid carcinoma of the nasopharynx KB cells assessed as growth inhibition incubated for 72 hrs by sulforhodamine B colorimetric assay. Cytotoxicity against human epidermoid carcinoma of the nasopharynx KB cells assessed as growth inhibition incubated for 72 hrs by sulforhodamine B colorimetric assay.	23883077

In Vitro

Schisanlactone B (C1) (5-10 μM; 24 h) down-regulates intracellular GST protein levels in a concentration-dependent manner in both HepG2 and HepG2/DDP cells^[1].
Schisanlactone B (10 μM; 6 h), in combination with Cisplatin, increases ROS levels in both HepG2 and HepG2/DDP cells^[1].
Schisanlactone B (20 μM; 30 min) is a natural GST inhibitor that inhibits purified GST activity with an IC₅₀ of 5 μM, binding to GST via Van der Waals interactions at PRO A:73 and GLU A:85^[1].
Schisanlactone B (C1) (5 μM; 24 h) effectively reduces intracellular GST levels in both HepG2/DDP and HepG2 cells, as demonstrated by decreased fluorescence imaging signals^[1].
Schisanlactone B (2.5-20 μM; 48 h) decreases cell viability in a concentration-dependent manner in HepG2 (IC₅₀ = 17.2 μM) and HepG2/DDP (IC₅₀ = 14.3 μM) cells^[1].
Schisanlactone B (Compound 13) (1 nM-100 μM; 48 h) exhibits cytotoxic activity against HL-60 cells with an IC₅₀ of 34.72 μM, and shows no activity against Bel-7402, BGC-823, and MCF-7 cell lines^[2].
Schisanlactone B (Compound 2) (0.5-100 µg/mL; 24 h) exhibits moderate cytotoxic activity against murine leukemia (CCRF-CEM) cells with an IC₅₀ of 4.66 µg/mL and against Hela cells with an IC₅₀ of 46.6 µg/mL^[3].
Schisanlactone B (compound 6) exhibits potent antiproliferative activity against NCI-H23, HCT-15, NUGC-3, ACHN, PC-3, and MDA-MB-231 human cancer cell lines with GI₅₀ values in the low micromolar range^[4].
Schisanlactone B (up to 20 mg/mL; 72 h) exhibits moderate cytotoxicity against A549, PC-3, KB and KBvin human cancer cell lines with GI₅₀ values ranging from 15.02 to 18.09 μM^[6].
Schisanlactone B (7.5 μM; 48 h) induces apoptosis in a concentration-dependent manner in HepG2 and HepG2/DDP cells^[1].
Schisanlactone B (5-10 μM; 24 h) modulates apoptosis-related protein expression by increasing C-caspase-3 and Bax and decreasing P-caspase 3 and Bcl-2 in HepG2/DDP cells^[1].
Schisanlactone B (10 μM; 48 h), in combination with Cisplatin (HY-17394), induces cell cycle arrest at G2 phase in HepG2 cells and G1 phase in HepG2/DDP cells^[1].
Schisanlactone B (10 μM; 24 h), in combination with Cisplatin, induces mitochondrial membrane damage, with stronger effects in HepG2/DDP cells compared to HepG2 cells^[1].
Schisanlactone B (10 μM; 24 h) regulates mitochondrial apoptosis-related proteins (caspase 3, Bax, Bcl-2, Cyt C) and down-regulates GST expression in both HepG2 and HepG2/DDP cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[1]

Cell Line:

HepG2/DDP and HepG2
Concentration:

5 μM; 10 μM
Incubation Time:

24 h
Result:

Down-regulated GST protein levels in a concentration-dependent manner in both HepG2 and HepG2/DDP cells.

Immunofluorescence^[1]

Cell Line:

HepG2/DDP and HepG2
Concentration:

5 μM
Incubation Time:

24 h (C1); 30 min (NEM); 20 min (staining)
Result:

Reduced intracellular GST levels in both HepG2/DDP and HepG2 cells, as demonstrated by decreased fluorescence imaging signals.

Cell Viability Assay^[1]

Cell Line:

HepG2 and HepG2/DDP
Concentration:

2.5 μM; 5 μM; 7.5 μM; 10 μM; 15 μM; 20 μM
Incubation Time:

48 h (C1); 4 h (MTT)
Result:

Decreased cell viability in a concentration-dependent manner in HepG2 and HepG2/DDP cells with an IC₅₀ of 17.2 μM in HepG2 and an IC₅₀ of 14.3 μM in HepG2/DDP cells.

Apoptosis Analysis^[1]

Cell Line:

HepG2 and HepG2/DDP
Concentration:

7.5 μM
Incubation Time:

48 h
Result:

Induced apoptosis in a concentration-dependent manner in both HepG2 and HepG2/DDP cells.
Exhibited a higher apoptotic rate in HepG2/DDP cells (18.9%) compared to HepG2 cells (13.8%) at 7.5 μM.

Western Blot Analysis^[1]

Cell Line:

HepG2/DDP and HepG2
Concentration:

5 μM; 7.5 μM; 10 μM
Incubation Time:

24 h
Result:

Increased the levels of cleaved caspase-3 (C-caspase-3) and Bax, but decreased the expression of P-caspase 3 and Bcl-2 in HepG2/DDP cells.

Cell Cycle Analysis^[1]

Cell Line:

HepG2 and HepG2/DDP
Concentration:

10 μM
Incubation Time:

48 h
Result:

Induced cell cycle arrest at G2 phase in HepG2 cells and G1 phase in HepG2/DDP cells in combination with Cisplatin.

Immunofluorescence^[1]

Cell Line:

HepG2 and HepG2/DDP
Concentration:

10 μM
Incubation Time:

24 h
Result:

Induced mitochondrial membrane damage in combination with Cisplatin, with stronger effects in HepG2/DDP cells compared to HepG2 cells.

Western Blot Analysis^[1]

Cell Line:

HepG2 and HepG2/DDP
Concentration:

10 μM
Incubation Time:

24 h
Result:

Regulated mitochondrial apoptosis-related proteins (caspase 3, Bax, Bcl-2, Cyt C) and down-regulated GST expression in both HepG2 and HepG2/DDP cells.

In Vivo

Schisanlactone B (C1) (5 mg/kg; in situ injection; single dose) effectively down-regulates GST levels in vivo in both Cisplatin-resistant and Cisplatin-sensitive HCC mouse models^[1].
C1 (10 mg/kg; i.p.; once every 2 days; 16 days) achieves a tumor inhibition rate of 19.4% in HepG2/DDP tumor-bearing mice, and C1 (5 mg/kg) combined with Cisplatin (2.5 mg/kg) achieves a tumor inhibition rate of 71.7%, demonstrating effective sensitization of Cisplatin-resistant HCC to Cisplatin^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

BALB/C nude mice (female, 6-8 weeks, 18-20 g)^[1]
Dosage:

5 mg/kg
Administration:

in situ injection; single dose
Result:

Down-regulated GST levels in vivo in both Cisplatin-resistant (HepG2/DDP) and Cisplatin-sensitive (HepG2) hepatocellular carcinoma mouse models.

Animal Model:

BALB/C nude mice (female)^[1]
Dosage:

10 mg/kg (monotherapy); 5 mg/kg (combination with Cisplatin)
Administration:

i.p.; once every 2 days; 16 days
Result:

Achieved a tumor inhibition rate of 19.4% as a single agent.
Achieved a tumor inhibition rate of 71.7% in combination with Cisplatin (2.5 mg/kg).
Induced extensive cell death and mitochondrial apoptosis by up-regulating Bax, C-caspase 3, and Cyt C and down-regulating Bcl-2 and GST.

Related Protocols :

Chemical Information

CAS No. 87164-32-7
분자량 466.66
화학식 C₃₀H₄₂O₄
SMILES

C[C@]12[C@]3([C@]4([C@]5(C4)[C@@](CC3)(C(C)(C)OC(=O)C=C5)[H])CC[C@]1(C)[C@@]([C@H](C)[C@]6(OC(=O)C(C)=CC6)[H])(CC2)[H])[H]
Structure Classification
- Terpenoids
- Pentacyclic Triterpenoids
Initial Source
선적

Room temperature in continental US; may vary elsewhere.
보관

Please store the product under the recommended conditions in the Certificate of Analysis.

순도&문서

Handling Instructions (2659 KB)

References

[1]. Mao L, et al. Rapid discovery of a novel "green" and natural GST inhibitor for sensitizing hepatocellular carcinoma to Cisplatin by visual screening strategy. Journal of pharmaceutical analysis. 2024 May;14(5):100923.

[2]. Wang W, et al. New triterpenoids from Kadsura heteroclita and their cytotoxic activity. Planta medica. 2006 Apr;72(5):450-7. [Content Brief]

[3]. Chen YG, et al. Triterpenoids from Schisandra henryi with cytotoxic effect on leukemia and Hela cells in vitro. Archives of pharmacal research. 2003 Nov;26(11):912-6.

[4]. Tram LH. A new triterpenoid from the stems of Kadsura coccinea with antiproliferative activity. Natural product research. 2022 May 23;36(10):2542-6.

[5]. Yu HY, et al. Triterpenoids from the fruit of Schisandra glaucescens. Fitoterapia. 2016 Sep;113:64-8.

[6]. Lu Y, et al. Cytotoxic and potential anticancer constituents from the stems of Schisandra pubescens. Pharmaceutical biology. 2013 Sep;51(9):1204-7. [Content Brief]

Calculators

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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Schisanlactone B