BPTES is an allosteric and selective glutaminase inhibitor with an IC₅₀ of 0.16 μM.

Glutaminase^[1]

BPTES (10 μM) exhibits inhibition of PDAC cell proliferation^[1]. BPTES preferentially slows growth of mutant IDH1 cells without inducing apoptosis. BPTES (10 μM) reduces glutaminase activity in both WT and mutant IDH1 expressing cells, diminishes glutamate and α-KG levels, and increases glycolytic intermediates while leaving total 2-HG levels unaffected^[2]. BPTES (10 μM) shows a clear synergistic anti-cancer effect with 10 μM of 5-FU in A549 and EKVX cell lines, and results in a growth reduction response not only in EKVX and A549 but also in most of the NSCLC cell lines^[3]. BPTES (10 μM) effectively reduces the levels of the metabolites of the TCA cycle, with no changes in the levels of metabolites in glycolysis and the pentose phosphate pathway. BPTES treatment reduces about 30% ATP production under normoxia, and an additional 10% reduction of ATP production is observed under hypoxia in EKVX^[4].

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

BPTES-NPs (BPTES nanoparticles, 1.2 mg BPTES in 100 μL nanoparticles, i.v.) significantly attenuates tumor growth in the patient-derived pancreatic orthotopic tumor model^[1].

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

524.68

C₂₄H₂₄N₆O₂S₃

314045-39-1

Solid

White to off-white

O=C(NC1=NN=C(CCSCCC2=NN=C(NC(CC3=CC=CC=C3)=O)S2)S1)CC4=CC=CC=C4

Room temperature in continental US; may vary elsewhere.

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.

• [1]. Elgogary A, et al. Combination therapy with BPTES nanoparticles and targets the metabolic heterogeneity of pancreatic cancer. Proc Natl Acad Sci U S A. 2016 Sep 6;113(36):E5328-36.  [Content Brief]

  [2]. Meghan J. Seltzer, et al. Inhibition of glutaminase preferentially slows growth of glioma cells with mutant IDH1. Cancer Res. 2010 Nov 15; 70(22): 8981-8987.  [Content Brief]

  [3]. Lee JS, et al. Glutaminase 1 inhibition reduces thymidine synthesis in NSCLC. Biochem Biophys Res Commun. 2016 Aug 26;477(3):374-82  [Content Brief]

  [4]. Lee JS, et al. Dual targeting of glutaminase 1 and thymidylate synthase elicits death synergistically in NSCLC. Cell Death Dis. 2016 Dec 8;7(12):e2511.  [Content Brief]