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Cantrixil

Catalog No. T39586   CAS 2135511-22-5
Synonyms: TRX-E-002-1

Cantrixil (TRX-E-002-1) is a second-generation super-benzopyran (SBP) compound, derived from TRX-E-002. It elicits an increase in phosphorylated c-Jun levels, leading to caspase-mediated apoptosis in ovarian cancer cells. Cantrixil exhibits potent pan anti-cancer activity against various cancer phenotypes.

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Cantrixil Chemical Structure
Cantrixil, CAS 2135511-22-5
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Description Cantrixil (TRX-E-002-1) is a second-generation super-benzopyran (SBP) compound, derived from TRX-E-002. It elicits an increase in phosphorylated c-Jun levels, leading to caspase-mediated apoptosis in ovarian cancer cells. Cantrixil exhibits potent pan anti-cancer activity against various cancer phenotypes.
In vitro TRX-E-002-1 exhibits extensive cytotoxic effects against ovarian, prostate, and lung cancer cell lines, demonstrating potent IC 50 values (SK-OV-3, JAM, OVCAR-3: 0.023-0.065 μM; DU145, PC3, C4-2B: 0.014-0.096 μM; A549: 0.058 μM). However, its effectiveness varies more in pancreatic, colorectal cancer, and glioblastoma cells[1]. As Cantrixil, at a concentration of 0.2 μM over 2-24 hours, it significantly increases phosphorylated c-Jun (p-c-Jun) levels while decreasing phosphorylated-ERK (p-ERK) levels[2]. Furthermore, at 2.45 μM for the same duration, Cantrixil substantially elevates caspase-3/7 and caspase-9 activities, particularly after 16 and 24 hours[2]. TRX-E-002-1 also inhibits a range of cytochrome P450 enzymes critical for drug metabolism (CYP2C9, CYP2C8, CYP2C19, CYP2B6, CYP3A4, CYP2D6, CYP2A6, CYP1A2), with IC 50 values spanning 1.5 to 75 μM (612-30,600 ng/mL)[1]. Western blot analysis on ovarian cancer stem cells (OCSCs) treated with 0.2 μM Cantrixil for 2-24 hours indicates increased p-c-Jun and decreased p-ERK levels, alongside a time-dependent rise in both total and phosphorylated c-Jun[2].
In vivo TRX-E-002-1 administered intraperitoneally (IP) at a dose of 100 mg/kg/day significantly suppresses tumor growth and reduces terminal tumor burden across several mouse models of cancer. In the disseminated ovarian cancer model, treatment for 13-14 days inhibited tumor growth. In the recurrent ovarian cancer model, a 4-week treatment regimen decreased tumor growth, reducing the terminal tumor burden by 77%. When administered for 18 days, TRX-E-002-1 notably decreased the terminal pancreatic tumor burden in a model using human Panc-1 pancreatic tumor cells implanted orthotopically in female NOD-SCID mice. Additionally, pharmacokinetic analysis in both male and female Sprague-Dawley rats revealed a half-life (T 1/2) of 2.5 hours, a peak concentration (C max) of 8355 ng/mL, and an area under the curve (AUC 0-∞) of 40600 ng?h/mL. In the disseminated ovarian cancer mouse model, a similar dosage led to a significant reduction in tumor growth and a 50-72% decrease in excised tumor weight at study's end.
Synonyms TRX-E-002-1
Molecular Weight 408.45
Formula C24H24O6
CAS No. 2135511-22-5

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

TargetMolReferences and Literature

1. Muhammad Wasif Saif, et al. Pharmacology and toxicology of the novel investigational agent Cantrixil (TRX-E-002-1). Cancer Chemother Pharmacol. 2017 Feb;79(2):303-314. 2. Ayesha B Alvero, et al. TRX-E-002-1 Induces c-Jun-Dependent Apoptosis in Ovarian Cancer Stem Cells and Prevents Recurrence In Vivo. Mol Cancer Ther. 2016 Jun;15(6):1279-90.

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Keywords

Cantrixil 2135511-22-5 TRX-E-002-1 inhibitor inhibit

 

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