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PX-12
PX-12 Chemical Structure

PX-12

Catalog NO.: 141400-58-0 CAS NO.: 141400-58-0 Brand: BOC Sciences

Category
Inhibitor
Tag/Targets
Antiangiogenic
Molecular Formula
C7H12N2S2
Molecular Weight
188.31

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WARNING: Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

cGMP Capacity

  • kg to MT scale
  • GMP batches production
  • Over 20 years of experience
  • HPAPI production with OEL < 1 μg/m³
  • Cleanroom Class 100 to Class 100,000
  • Special type of reactions in cGMP workshop
  • Cleaning level: Class A B C
  • cGMP synthesis workshop
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Product Description

PX-12 is an irreversible inhibitor of Trx-1 currently in clinical development as an antitumor agent. The research results suggest that the lowering of elevated levels of plasma Trx-1 in cancer patients may provide a surrogate for the inhibition of tumor Trx-1 by PX-12.

InChI Key
BPBPYQWMFCTCNG-UHFFFAOYSA-N
InChI
InChI=1S/C7H12N2S2/c1-3-6(2)10-11-7-8-4-5-9-7/h4-6H,3H2,1-2H3,(H,8,9)
SMILES
CCC(C)SSC1=NC=CN1
Current Developer
Biomira Inc; Oncothyreon Inc.
NCT NumberTitleCondition Or DiseasePhaseStart DateSponsorStatus
NCT00417287Phase II Study of PX-12 in Patients With Advanced Pancreatic CancerPancreatic NeoplasmsPhase 2December 2006Cascadian Therapeutics Inc.Terminated
NCT00736372A Trial of PX-12 in Patients With a Histologically or Cytologically Confirmed Diagnosis of Advanced or Metastatic CancerMetastatic CancerPhase 1June 2008Cascadian Therapeutics Inc.Completed
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1.Thioredoxin-1 inhibitor PX-12 induces human acute myeloid leukemia cell apoptosis and enhances the sensitivity of cells to arsenic trioxide.
Tan Y1, Bi L2, Zhang P1, Wang F1, Lin F1, Ni W3, Wu J1, Jiang L1. Int J Clin Exp Pathol. 2014 Jul 15;7(8):4765-73. eCollection 2014.
Thioredoxin-1 (Trx-1), an important redox regulatory factor, plays a significant role in drug-induced apoptosis. Here we investigated the effects of the Trx-1 inhibitor 1-methylpropyl 2-imidazolyl disulfide (PX-12) on human acute myeloid leukemia cells (AML) and the sensitivity of cells to arsenic trioxide (As2O3, ATO). Treatment of cells with a different concentration of PX-12 for 48 h resulted in growth inhibition, the induction of apoptosis and increased the levels of activated caspase-3 expression in AML cell lines HL-60, NB4, U937 and primary AML cells in a dose-dependent manner. In addition, PX-12 enhanced the sensitivity of U937 cells to ATO. These results suggest the effects of Trx-1 inhibitor PX-12 to induce apoptosis in AML cells and therapeutic potential in AML by enhancing the sensitivity of cells to ATO.
2.Upregulation of connexin43 contributes to PX-12-induced oxidative cell death.
Li G1,2,3, Gao K1, Chi Y1, Zhang X1, Mitsui T2, Yao J4, Takeda M2. Tumour Biol. 2015 Dec 18. [Epub ahead of print]
Thioredoxin (Trx) is a small redox protein that underlies aggressive tumor growth and resistance to chemotherapy. Inhibition of Trx with the chemical inhibitor PX-12 suppresses tumor growth and induces cell apoptosis. Currently, the mechanism underlying the therapeutic actions of PX-12 and the molecules influencing cell susceptibility to PX-12 are incompletely understood. Given that connexin43 (Cx43), a tumor suppressor, regulates tumor cell susceptibility to chemotherapy, we examined the possible involvement of Cx43 in PX-12-induced cell death. Exposure of cells to PX-12 led to a loss of cell viability, which was associated with the activation of oxidative sensitive c-Jun N-terminal kinase (JNK). Inhibition of JNK or supplement of cells with anti-oxidants prevented the cell-killing action of PX-12. The forced expression of Cx43 in normal and tumor cells increased cell sensitivity to PX-12-induced JNK activation and cell death. In contrast, the downregulation of Cx43 with siRNA or the suppression of gap junctions with chemical inhibitors attenuated JNK activation and enhanced cell resistance to PX-12.
3.Baseline [18F]FMISO μPET as a Predictive Biomarker for Response to HIF-1α Inhibition Combined with 5-FU Chemotherapy in a Human Colorectal Cancer Xenograft Model.
De Bruycker S1, Vangestel C1,2, Van den Wyngaert T1,2, Wyffels L1,2, Wouters A3, Pauwels P3, Staelens S1, Stroobants S4,5. Mol Imaging Biol. 2016 Jan 4. [Epub ahead of print]
PURPOSE: The purpose of this study was to characterize imaging biomarkers for the potential benefit of hypoxia-inducible factor-1 (HIF-1)α inhibition (by PX-12) during 5-fluorouracil (5-FU) chemotherapy in the treatment of colorectal cancer (CRC).
4.Hypoxia inducible factor-1α inhibition produced anti-allodynia effect and suppressed inflammatory cytokine production in early stage of mouse complex regional pain syndrome model.
Hsiao HT1,2, Lin YC1, Wang JC1, Tsai YC1, Liu YC1. Clin Exp Pharmacol Physiol. 2016 Mar;43(3):355-9. doi: 10.1111/1440-1681.12536.
Complex regional pain syndrome (CRPS) is related to microcirculation impairment associated with tissue hypoxia and peripheral cytokine overproduction in the affected limb. Previous studies suggest that the pathogenesis involves hypoxia inducible factor-1α (HIF-1α) and exaggerated regional inflammatory response. 1-methylpropyl 2-imidazolyl disulfide (PX-12) acts as the thioredoxin-1 (Trx-1) inhibitor and decreases the level of HIF-1α, and can rapidly be metabolized for Trx-1 redox inactivation. This study hypothesized that PX-12 can decrease the cytokine production for nociceptive sensitization in the hypoxia-induced pain model. CD1 mice weighing around 30 g were used. The animal CRPS model was developed via the chronic post-ischaemic pain (CPIP) model. The model was induced by using O-rings on the ankles of the mice hind limbs to produce 3-h ischaemia-reperfusion injury on the paw. PX-12 (25 mg/kg, 5 mg/kg) was given through tail vein injection immediately after ischaemia.
Preparing Stock Solutions
ConcentrationVolumeMass1 mg5 mg10 mg
1 mM5.3104 mL26.5520 mL53.1039 mL
5 mM1.0621 mL5.3104 mL10.6208 mL
10 mM0.5310 mL2.6552 mL5.3104 mL
50 mM0.1062 mL0.5310 mL1.0621 mL
About Us

BOC Sciences is a trusted global supplier of research chemicals, biochemicals, and pharmaceutical ingredients, serving the life sciences, biotech, and pharmaceutical industries. Headquartered in New York, we offer a comprehensive product portfolio that includes inhibitors, building blocks, carbohydrates, nucleosides, nucleotides, GMP products, impurities and metabolites, APIs, natural compounds, ADC-related chemicals, and stem cell molecules.

We specialize in the synthesis, biosynthesis, purification, and characterization of small molecules. With years of industry experience, our scientific and technical teams support projects ranging from early discovery to process development and regulatory submission.

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