Drug (ID: DG01487) and It's Reported Resistant Information
Name
BPTES
Synonyms
BPTES; 314045-39-1; Bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide; 3uo9; N,N'-[sulfanediylbis(Ethane-2,1-Diyl-1,3,4-Thiadiazole-5,2-Diyl)]bis(2-Phenylacetamide); CHEMBL2177757; 2,2'-(5,5'-(2,2'-thiobis(ethane-2,1-diyl))bis(1,3,4-thiadiazole-5,2-diyl))bis(azanediyl)bis(1-phenylethanone); 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; N,N'-((thiobis(ethane-2,1-diyl))bis(1,3,4-thiadiazole-5,2-diyl))bis(2-phenylacetamide); 2-phenyl-N-{5-[2-({2-[5-(2-phenylacetamido)-1,3,4-thiadiazol-2-yl]ethyl}sulfanyl)ethyl]-1,3,4-thiadiazol-2-yl}acetamide; 4jkt; 04A; SCHEMBL2640644; Glutaminase Inhibitor II, BPTES; SNX1770; HMS3866K13; BCP15991; BPTES, >=95% (HPLC); EX-A2297; SNX-1770; ZINC4426660; BDBM50400050; MFCD01079848; NSC798303; s7753; AKOS027470168; CCG-269883; CS-4586; NSC-798303; NCGC00420698-04; AC-29967; AS-70948; HY-12683; A14954; US8604016, 1; Q27449834; Bis[2-[5-[(2-phenylacetyl)amino]-1,3,4-thiadiazole-2-yl]ethyl] sulfide; (N,N'-[thiobis(2,1-ethanediyl-1,3,4-thiadiazole-5,2-diyl)]bisbenzeneacetamide); N,N'-[Thiobis(2,1-ethanediyl-1,3,4-thiadiazole-5,2-diyl)]bis[benzeneacetamide]; N,N'-[Thiobis(2,1-ethanediyl-1,3,4-thiadiazole-5,2-diyl)]bisbenzeneacetamide; 2,2-(5,5-(2,2-thiobis(ethane-2,1-diyl))bis(1,3,4-thiadiazole-5,2-diyl))bis(azanediyl)bis(1-phenylethanone)
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Structure
Target . NOUNIPROTAC [1]
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Formula
12
IsoSMILES
C1=CC=C(C=C1)CC(=O)NC2=NN=C(S2)CCSCCC3=NN=C(S3)NC(=O)CC4=CC=CC=C4
InChI
InChI=1S/C24H24N6O2S3/c31-19(15-17-7-3-1-4-8-17)25-23-29-27-21(34-23)11-13-33-14-12-22-28-30-24(35-22)26-20(32)16-18-9-5-2-6-10-18/h1-10H,11-16H2,(H,25,29,31)(H,26,30,32)
InChIKey
MDJIPXYRSZHCFS-UHFFFAOYSA-N
PubChem CID
3372016
Type(s) of Resistant Mechanism of This Drug
  UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Their Corresponding Diseases
ICD-02: Benign/in-situ/malignant neoplasm
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Brain cancer [ICD-11: 2A00]
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Unusual Activation of Pro-survival Pathway (UAPP) Click to Show/Hide
Key Molecule: Oxalosuccinate decarboxylase (IDH1) [2]
Molecule Alteration Missense mutation
p.R132H (c.395G>A)
Sensitive Disease Brain glioma [ICD-11: 2A00.0]
Experimental Note Revealed Based on the Cell Line Data
Experiment for
Drug Resistance
3H-thymidine incorporation assay
Mechanism Description The missense mutation p.R132H (c.395G>A) in gene IDH1 cause the sensitivity of BPTES by unusual activation of pro-survival pathway
Acute myeloid leukemia [ICD-11: 2A60]
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Unusual Activation of Pro-survival Pathway (UAPP) Click to Show/Hide
Key Molecule: Oxalosuccinate decarboxylase (IDH1) [1]
Molecule Alteration Missense mutation
p.R132C (c.394C>T)
Sensitive Disease Acute myeloid leukemia [ICD-11: 2A60.0]
Experimental Note Identified from the Human Clinical Data
In Vitro Model 5637 cells Bladder Homo sapiens (Human) CVCL_0126
AML cells N.A. Homo sapiens (Human) N.A.
Experiment for
Drug Resistance
Manually cell counting assay
References
Ref 1 Inhibition of glutaminase selectively suppresses the growth of primary acute myeloid leukemia cells with IDH mutationsExp Hematol. 2014 Apr;42(4):247-51. doi: 10.1016/j.exphem.2013.12.001. Epub 2013 Dec 11.
Ref 2 Inhibition of glutaminase preferentially slows growth of glioma cells with mutant IDH1Cancer Res. 2010 Nov 15;70(22):8981-7. doi: 10.1158/0008-5472.CAN-10-1666. Epub 2010 Nov 2.

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