1. Metabolic Enzyme/Protease Apoptosis
  2. Lipoxygenase Caspase Apoptosis
  3. Lycopodine

Lycopodine, a pharmacologically important bioactive component derived from Lycopodium clavatumspores, triggers apoptosis by modulating 5-lipoxygenase, and depolarizing mitochondrial membrane potential in refractory prostate cancer cells without modulating p53 activity. Lycopodine inhibits proliferation of HeLa cells through induction of apoptosis via caspase-3 activation.

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Lycopodine Chemical Structure

Lycopodine Chemical Structure

CAS No. : 466-61-5

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Description

Lycopodine, a pharmacologically important bioactive component derived from Lycopodium clavatumspores, triggers apoptosis by modulating 5-lipoxygenase, and depolarizing mitochondrial membrane potential in refractory prostate cancer cells without modulating p53 activity[1]. Lycopodine inhibits proliferation of HeLa cells through induction of apoptosis via caspase-3 activation[2].

IC50 & Target[2]

Caspase-3

 

5-Lipoxygenase

 

In Vitro

Lycopodine (5.22-78.3 μg/mL; 12 hours) has 50% viability at 57.62±0.086 μg/mL and 51.46±1.43 μg/mL for PC3 and LnCaP, respectively[1].
Treated with Lycopodine (74-222 mM; 12 hours), the apoptotic index is with respect to the gradual increase in doses for the PC3 and LnCaP cells[1].
Lycopodine (74-222 mM; 12 hours) induces cell cycle arrest at G0/G1 phase in PC3 and LnCaP cells[1].
Lycopodine (0-200 µg/mL; 48 hours) shows cytotoxicity to HeLa cells in a dose and time dependent manner. However, Lycopodine shows minimal cytotoxic effects in normal peripheral blood mononuclear cells (PBMC) even at the highest dose (200 µg/mL)[2].
Lycopodine (100, 200 µg/mL; 24 hours) increases level of Bax and decreases the mitochondrial cytochrome c. This is followed by an increase in expression of cytochrome c in cytosolic fraction. Lycopodine also cleaves the caspase-3 in the total cell lysate, while the expression of Bcl-2 is down regulated[2].

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

Cell Viability Assay[1]

Cell Line: PC3 and LnCaP cells
Concentration: 5.22-78.3 μg/mL
Incubation Time: 12 hours
Result: Reached 50% viability at 57.62±0.086 μg/mL and 51.46±1.43 μg/mL for PC3 and LnCaP, respectively.

Apoptosis Analysis[1]

Cell Line: PC3 and LnCaP cells
Concentration: 74, 148, 222 mM
Incubation Time: 12 hours
Result: The apoptotic index was with respect to the gradual increase in doses.

Cell Cycle Analysis[1]

Cell Line: PC3 and LnCaP cells
Concentration: 74, 148, 222 mM
Incubation Time: 12 hours
Result: Arrested growth of the cells at G0/G1 phase in the case of PC3 and LnCaP cells.

Cell Cytotoxicity Assay[2]

Cell Line: Hela cells and PBMC
Concentration: 0-200 µg/mL
Incubation Time: 48 hours
Result: A linear increase of the cytotoxicity was along with the increase of time of treatment and also of the dose.

Western Blot Analysis[2]

Cell Line: HeLa cells
Concentration: 100, 200 µg/mL
Incubation Time: 24 hours
Result: Increased level of Bax and decreased the mitochondrial cytochrome c.
Molecular Weight

247.38

Formula

C16H25NO

CAS No.
SMILES

O=C1[C@]2([H])[C@]34[C@@](CCCN4CCC2)([H])[C@](C[C@@H](C)C3)([H])C1

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