2. Apoptosis Cell Cycle/DNA Damage Metabolic Enzyme/Protease
  3. Apoptosis DNA/RNA Synthesis Mitochondrial Metabolism
  4. Ganoderic acid T

Ganoderic acid T is a lanostane triterpenoid. Ganoderic acid T is isolated from Ganoderma lucidum mycelia. Ganoderic acid T induces Mitochondria-mediated Apoptosis and inhibits DNA synthesis. Ganoderic acid T exhibits anticancer activity against cervical cancer, liver cancer and lung cancer.

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Ganoderic acid T

Ganoderic acid T Chemical Structure

CAS No. : 103992-91-2

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Description

Ganoderic acid T is a lanostane triterpenoid. Ganoderic acid T is isolated from Ganoderma lucidum mycelia. Ganoderic acid T induces Mitochondria-mediated Apoptosis and inhibits DNA synthesis. Ganoderic acid T exhibits anticancer activity against cervical cancer, liver cancer and lung cancer[1][2][3][4].

Cellular Effect
Cell Line Type Value Description References
Vero IC50
28 μM
Compound: 37
Cytotoxicity against African green monkey Vero cells by green fluorescent protein microplate assay
Cytotoxicity against African green monkey Vero cells by green fluorescent protein microplate assay
[PMID: 26716912]
In Vitro

Ganoderic acid T (6-50 μg/mL; 24 h) inhibits the proliferation of cancer cell lines (95-D, SMMC7721, KB-A-1, KB-3-1, HeLa) and normal cell lines (HLF, L-02) in a dose-dependent manner, with the strongest inhibitory activity against 95-D cells (IC50 = 27.9 μg/mL)[1].
Ganoderic acid T (2-10 μg/mL; 12 days) dose-dependently inhibits colony formation of 95-D cells, with an EC50 of 3.34 μg/mL[1].
Ganoderic acid T (50 μg/mL; 4-8 h) induces time-dependent apoptosis in 95-D cells[1].
Ganoderic acid T (25-50 μg/mL; 24 h) induces G1 cell cycle arrest in 95-D cells in a dose-dependent manner, with 76% of cells arrested at the G1 phase after treatment with 50 μg/mL for 24 h[1].
Ganoderic acid T (0-40 μM; 24 h) potently inhibits the viability of cervical cancer HeLa cells, liver cancer HepG2 cells, and lung cancer 95-D cells (with an IC50 of 11.0 μM in HeLa cells), and exhibits significantly lower cytotoxicity toward non-tumorigenic MCF-10A cells[3].
Ganoderic acid T (5-40 μM; 24 h) inhibits DNA synthesis in cervical cancer HeLa cells in a dose-dependent manner[3].
Ganoderic acid T (5-20 μM; 24 h) dose-dependently arrests cervical cancer HeLa cells at the G1 phase and increases the sub-G1 apoptotic cell population, with 55.30% of cells in the G1 phase and 17.33% in the sub-G1 phase, while exerting only minimal effects on non-tumorigenic MCF-10A cells[3].
Ganoderic acid T (5-20 μM; 24 h) induces apoptosis in cervical cancer HeLa cells in a dose-dependent manner, while it causes only minimal apoptosis in non-tumorigenic MCF-10A cells[3].

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

Ganoderic acid T Related Antibodies

Cell Proliferation Assay[1]

Cell Line: human highly metastatic lung tumor cell line 95-D, human liver tumor cell line SMMC7721, human epidermal cancer cell lines KB-A-1 and KB-3-1, human cervixal cancer cell line HeLa, human normal cell lines HLF (lung) and L-02 (liver)
Concentration: 6-50 μg/mL; 10-50 μg/mL (95-D-specific analysis)
Incubation Time: 24 h
Result: Reduced proliferation of multiple cancer cell lines in a dose-dependent manner, with higher cytotoxicity to 95-D cells than to normal cell lines.
Suppressed 95-D cell viability by 70% at 50 μg/mL after 24 h, with an IC50 of 27.9 μg/mL.

Apoptosis Analysis[1]

Cell Line: human highly metastatic lung tumor cell line 95-D
Concentration: 50 μg/mL
Incubation Time: 4 h, 8 h
Result: Induced apoptosis in 95-D cells in a time-dependent manner.
Increased total apoptotic cell percentage (early + late apoptosis) to 36.5% after 4 h of treatment with 50 μg/mL.
Resulted in apoptosis in ~50% of the cells after 8 h of treatment with 50 μg/mL.

Cell Cycle Analysis[1]

Cell Line: human highly metastatic lung tumor cell line 95-D
Concentration: 25-50 μg/mL
Incubation Time: 24 h
Result: Induced G1 phase cell cycle arrest in 95-D cells in a dose-dependent manner.
Increased the percentage of cells in G1 phase from 48% (control) to 76% at 50 μg/mL for 24 h.
Decreased the percentage of cells in S phase from 37% (control) to 13% at 50 μg/mL for 24 h.

Cell Cycle Analysis[3]

Cell Line: human cervical cancer HeLa cells, non-tumorous human breast epithelial MCF-10A cells
Concentration: 5 μM, 10 μM, 20 μM
Incubation Time: 24 h
Result: Caused dose-dependent accumulation in the G1 phase in HeLa cells: 44.54% at 5 μM, 46.47% at 10 μM, and 55.30% at 20 μM (compared to 42.53% in control).
Induced a dose-dependent increase in the sub-G1 apoptotic population in HeLa cells: 1.52% at 5 μM, 7.47% at 10 μM, and 17.33% at 20 μM (compared to 0.34% in control).
Caused only minimal changes in MCF-10A cells treated with 20 μM: the G1 phase increased slightly to 72.00% (compared to 66.20% in control), and the sub-G1 population only increased to 1.05% (compared to 0.66% in control).

Apoptosis Analysis[3]

Cell Line: human cervical cancer HeLa cells, non-tumorous human breast epithelial MCF-10A cells
Concentration: 5 μM, 10 μM, 20 μM
Incubation Time: 24 h
Result: Caused a dose-dependent increase in total apoptotic cells (early + late) in HeLa cells: 5.25% at 5 μM, 7.75% at 10 μM, and 11.12% at 20 μM (compared to 0.24% in control).
Increased early apoptotic cells to 3.69% and late apoptotic cells to 7.43% at 20 μM (compared to 99.77% viable cells in control).
Caused only minimal apoptosis in MCF-10A cells treated with 20 μM: total apoptotic cells increased slightly to 2.60%, with viable cells remaining at 97.20%.
In Vivo

Ganoderic acid T (12.5-25 mg/kg; i.p.; once daily; for 12 consecutive days) inhibits the growth of lung cancer xenografts in athymic mice[1].

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

Animal Model: BALB/c nude (4-week-old male, athymic, specific-pathogen-free, implanted with human highly metastatic lung cancer 95-D cells via two-step xenograft)[1]
Dosage: 12.5 mg/kg; 25 mg/kg
Administration: i.p.; daily; 12 days
Result: Achieved a tumor growth inhibition ratio of ~30% at 12.5 mg/kg.
Achieved a tumor growth inhibition ratio of ~60% at 25 mg/kg.
Molecular Weight

612.79

Formula

C36H52O8
CAS No.
SMILES

C[C@]12C3=CC[C@](C(C)([C@@H](CC4)OC(C)=O)C)([H])[C@@]4(C)C3=CC[C@@]1([C@@](C[C@@H]2OC(C)=O)([H])[C@H](C)[C@@H](OC(C)=O)C/C=C(C)/C(O)=O)C
Structure Classification
Initial Source

cultured mycelia of G. lucidum.
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Ganoderic acid T Related Classifications

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Ganoderic acid T103992-91-2ApoptosisDNA/RNA SynthesisMitochondrial Metabolismp53Baxlung cancerSMMC7721Ganoderma lucidumapoptosis95-Dcaspase-3cell cycleHeLaInhibitorinhibitorinhibit

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