1. Apoptosis
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  3. Cantrixil

Cantrixil (Synonyms: TRX-E-002-1)

Cat. No.: HY-114250
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Cantrixil (TRX-E-002-1), an active enantiomer of TRX-E-002, is a second-generation super-benzopyran (SBP) compound. Cantrixil increases phosphorylated c-Jun levels resulting in caspase-mediated apoptosis in ovarian cancer cells. Cantrixil has potent pan anti-cancer activity against a broad range of cancer phenotypes.

For research use only. We do not sell to patients.

Cantrixil Chemical Structure

Cantrixil Chemical Structure

CAS No. : 2135511-22-5

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Description

Cantrixil (TRX-E-002-1), an active enantiomer of TRX-E-002, is a second-generation super-benzopyran (SBP) compound. Cantrixil increases phosphorylated c-Jun levels resulting in caspase-mediated apoptosis in ovarian cancer cells. Cantrixil has potent pan anti-cancer activity against a broad range of cancer phenotypes[1][2].

In Vitro

TRX-E-002-1 shows broad cytotoxic activity against ovarian, prostate and lung cancer cells, with IC50 values of ≤0.1 μM (SK-OV-3, JAM, OVCAR-3 cells: IC50=0.023-0.065 μM; DU145, PC3; C4-2B cells: IC50=0.014-0.096 μM; A549 cells: IC50=0.058 μM). Activity in pancreatic and colorectal cancer cells and glioblastoma cells are more variable[1].
Cantrixil (0.2 μM; 2-24 hours) shows high levels of phosphorylated c-Jun (p-c-Jun) and low levels of phosphorylated-ERK (p-ERK)[2].
Cantrixil (2.45 μM; 2-24 hours) induces a significant increase in both caspase-3/7 and caspase-9 activity at 16 and 24 hours[2].
TRX-E-002-1 inhibits multiple cytochrome P450 drug-metabolizing enzymes, including CYP2C9, CYP2C8, CYP2C19, CYP2B6, CYP3A4, CYP2D6, CYP2A6 and CYP1A2. IC50 values ranges from 1.5 to 75 μM (612-30,600 ng/mL)[1].

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

Western Blot Analysis[2]

Cell Line: Ovarian cancer stem cells (OCSCs)
Concentration: 0.2 μM
Incubation Time: 2, 4, 8, 16, 24 hours
Result: Showed higher levels of phosphorylated c-Jun (p-c-Jun) and lower levels of phosphorylated-ERK (p-ERK).
Showed a time-dependent increase in p-c-Jun accompanied by a time-dependent increase in total c-Jun.
In Vivo

TRX-E-002-1 (100 mg/kg/day; IP; for 13-14 days) significantly inhibits tumour growth in disseminated ovarian cancer mouse model[1].
TRX-E-002-1 (100 mg/kg/day; IP; for 4 weeks) inhibits tumour growth and reduces terminal tumour burden by 77% in the recurrent ovarian cancer mouse model[1].
TRX-E-002-1 (100 mg/kg/day; IP; for 18 days) significantly reduces terminal pancreatic tumour burden in a mouse model of pancreatic cancer (human Panc-1 pancreatic tumour cells implanted orthotopically into female NOD-SCID mice)[1].
TRX-E-002-1 (100 mg/kg; IP) has a T1/2 of 2.5 hours, a Cmax of 8355 ng/mL and an AUC0-∞ of 40600 ng•h/mL[1].

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

Animal Model: Disseminated ovarian cancer mouse model[1]
Dosage: 100 mg/kg (dissolved in 20% SBECD)
Administration: IP; once daily; for 13-14 days
Result: Significantly inhibited tumour growth and reduced excised tumour weight at termination by 50-72%.
Animal Model: Male female Sprague-Dawley rats[1]
Dosage: 100 mg/kg (Pharmacokinetic Analysis)
Administration: IP
Result: Had a T1/2 of 2.5 hours, a Cmax of 8355 ng/mL and an AUC0-∞ of 40600 ng•h/mL.
Molecular Weight

408.44

Formula

C₂₄H₂₄O₆

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Cantrixil
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