BPTES
Modify Date: 2024-01-03 16:52:58
BPTES structure
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Common Name | BPTES | ||
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| CAS Number | 314045-39-1 | Molecular Weight | 524.681 | |
| Density | 1.4±0.1 g/cm3 | Boiling Point | N/A | |
| Molecular Formula | C24H24N6O2S3 | Melting Point | N/A | |
| MSDS | Chinese USA | Flash Point | N/A | |
| Symbol |
GHS07 |
Signal Word | Warning | |
Use of BPTESBPTES is an allosteric and selective glutaminase inhibitor with an IC50 of 0.16 μM. |
| Name | 2-phenyl-N-[5-[2-[2-[5-[(2-phenylacetyl)amino]-1,3,4-thiadiazol-2-yl]ethylsulfanyl]ethyl]-1,3,4-thiadiazol-2-yl]acetamide |
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| Synonym | More Synonyms |
| Description | BPTES is an allosteric and selective glutaminase inhibitor with an IC50 of 0.16 μM. |
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| Related Catalog | |
| Target |
Glutaminase[1] |
| In Vitro | 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]. |
| In Vivo | 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]. |
| Kinase Assay | D54 cells are seeded in a T75 flask at 5×105 cells, and IDH1 expression is induced with doxycycline 48 hrs before assaying. Cells are collected and resuspended in PBS, 0.1% Triton X-100, and Halt-Protease Inhibitor. Cells are lysed for 30 min on ice and centrifuged for 30 min at 12000 rpm at 4°C. Protein concentration is measured using the BCA Assay. Varying amounts of protein are added to IDH activity assay buffer (33 mM Tris, pH 7.6, 0.33 mM EDTA, 0.1 mM NADP+, 1.33 mM MnCl2, and 1.3 mM isocitrate), and changes in absorbance at 340 nm after 5 min is documented for each protein amount. |
| Cell Assay | Cells are plated at a density of 500 cells/well in a 96-well black clear bottom plate. At 24 hrs, media is changed to the appropriate media (DMEM with 4.5 g/L, 1.5 g/L or 0.1 g/L glucose, 10% FBS, pencillin/streptomycin, and 4 mM glutamine with or without doxycyline). 48 hours after plating, compounds or DMSO are added. Media and alamarBlue is added to a volume of 200 µL in each well. Fluorescence is measured at 48 hrs or 72 hrs (EGCG) using a Victor3 plate-reader. |
| Animal Admin | Four-week-old female Foxn1nuathymic nude mice are used for the assay. Freshly resected pancreatic tumor samples obtained from patients at the time of surgery are propagated from mouse to mouse as a live tumor bank. Once a tumor volume of 50 mm3 is reached (4 wk postimplantation), mice are treated with 12.5 mg/kg BPTES by intraperitoneal injection, 200 mg/kg CB-839 twice per d by oral gavage, 54 mg/kg BPTES-NPs (1.2 mg BPTES in 100 µL nanoparticles per mouse) by intravenous injection, blank-NPs (100 µL per mouse) by intravenous injection, 25 mg/kg gemcitabine intraperitoneally, 250 mg/kg metformin intraperitoneally daily, or a combination of BPTES-NPs with gemcitabine or metformin. BPTES-NPs are injected once every 3 d for a total of six injections over 16 d. |
| References |
| Density | 1.4±0.1 g/cm3 |
|---|---|
| Molecular Formula | C24H24N6O2S3 |
| Molecular Weight | 524.681 |
| Exact Mass | 524.112305 |
| PSA | 198.52000 |
| LogP | 3.97 |
| Index of Refraction | 1.709 |
| Storage condition | -20℃ |
| Symbol |
GHS07 |
|---|---|
| Signal Word | Warning |
| Hazard Statements | H315-H319-H335 |
| Precautionary Statements | P261-P305 + P351 + P338 |
| RIDADR | NONH for all modes of transport |
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Protein Kinase A Activation Promotes Cancer Cell Resistance to Glucose Starvation and Anoikis.
PLoS Genet. 12 , e1005931, (2016) Cancer cells often rely on glycolysis to obtain energy and support anabolic growth. Several studies showed that glycolytic cells are susceptible to cell death when subjected to low glucose availabilit... |
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Increased glutamine catabolism mediates bone anabolism in response to WNT signaling.
J. Clin. Invest. 125(2) , 551-62, (2015) WNT signaling stimulates bone formation by increasing both the number of osteoblasts and their protein-synthesis activity. It is not clear how WNT augments the capacity of osteoblast progenitors to me... |
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Targeted inhibition of tumor-specific glutaminase diminishes cell-autonomous tumorigenesis.
J. Clin. Invest. 125 , 2293-306, (2015) Glutaminase (GLS), which converts glutamine to glutamate, plays a key role in cancer cell metabolism, growth, and proliferation. GLS is being explored as a cancer therapeutic target, but whether GLS i... |
| N,N'-[Sulfanediylbis(2,1-ethanediyl-1,3,4-thiadiazole-5,2-diyl)]bis(2-phenylacetamide) |
| bis-2-(5-Phenylacetmido-1,2,4-Thiadiazol-2-yl)Ethyl Sulfide |
| BPTES |
| 3uo9 |
| Benzeneacetamide, N,N'-[thiobis(2,1-ethanediyl-1,3,4-thiadiazole-5,2-diyl)]bis- |
| Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide |