Drug Information
Drug (ID: DG02039) and It's Reported Resistant Information
| Name |
10,12-Tricosadiynoic Acid
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| Synonyms |
10,12-Tricosadiynoic acid|66990-30-5|tricosa-10,12-diynoic acid|10,12-Tricosadiynoicacid|DTXSID40337084|10,12- Tricosadiynoic acid|SCHEMBL302150|DTXCID30288172|CHEBI:190947|MFCD00041683|AKOS015839844|10,12-Tricosadiynoic Acid, >/=98%|PD127433|HY-135425|CS-0112754|T1200|10,12-Tricosadiynoic acid, >=98.0% (GC)|D92469|677-355-9
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| Indication |
In total 1 Indication(s)
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| Structure |
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| Drug Resistance Disease(s) |
Disease(s) with Resistance Information Discovered by Cell Line Test for This Drug
(1 diseases)
[1]
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| Click to Show/Hide the Molecular Information and External Link(s) of This Drug | |||||
| Formula |
C23H38O2
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| IsoSMILES |
CCCCCCCCCCC#CC#CCCCCCCCCC(=O)O
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| InChI |
InChI=1S/C23H38O2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-20-21-22-23(24)25/h2-10,15-22H2,1H3,(H,24,25)
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| InChIKey |
DIEDVCMBPCRJFQ-UHFFFAOYSA-N
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| PubChem CID | |||||
Type(s) of Resistant Mechanism of This Drug
Drug Resistance Data Categorized by Their Corresponding Diseases
ICD-02: Benign/in-situ/malignant neoplasm
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Key Molecule: Acyl-CoA oxidase 1 (ACOX1) | [1] | |||
| Metabolic Type | Lipid metabolism | |||
| Resistant Disease | Chronic lymphocytic leukemia [ICD-11: 2A82.0] | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| In Vitro Model | HG3 cells | Blood | Homo sapiens (Human) | CVCL_Y547 |
| MEC1 cells | Blood | Homo sapiens (Human) | CVCL_1870 | |
| OSU-CLL cells | Blood | Homo sapiens (Human) | CVCL_Y382 | |
| PGA1 cells | Blood | Homo sapiens (Human) | CVCL_Y545 | |
| Primary B-lymphocytes cells | Blood | Homo sapiens (Human) | N.A. | |
| Experiment for Molecule Alteration |
qPCR, immunoblot and confocal microscopy approaches | |||
| Experiment for Drug Resistance |
Cell viability assay | |||
| Mechanism Description | Accordingly, downmodulation of ACOX1 (a rate-limiting pFAO enzyme overexpressed in CLL cells) was enough to shift the CLL cells' metabolism from lipids to a carbon- and amino-acid-based phenotype. Complete blockade of ACOX1 resulted in lipid droplet accumulation and caspase-dependent death in CLL cells, including those from individuals with poor cytogenetic and clinical prognostic factors. | |||
References
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