Drug (ID: DG00161) and It's Reported Resistant Information
Name
Epothilone B
Synonyms
Epothilone B; Patupilone; 152044-54-7; (-)-Epothilone B; Epo B; EpoB; EPO906; EPO 906; UNII-UEC0H0URSE; EPO 906A; GNF-PF-193; CHEBI:31550; UEC0H0URSE; AK163080; Epothilone B (EPO906, Patupilone); 7,11-DIHYDROXY-8,8,10,12,16-PENTAMETHYL-3-[1-METHYL-2-(2-METHYL-THIAZOL-4-YL)VINYL]-4,17-DIOXABICYCLO[14.1.0]HEPTADECANE-5,9-DIONE; Epothilon B; Patupilone [INN]; (1S,3S,7S,10R,11S,12S,16R)-7,11-dihydroxy-8,8,10,12,16-pentamethyl-3-((E)-1-(2-methylthiazol-4-yl)prop-1-en-2-yl)-4,17-dioxabicyclo[14.1.0]heptadecane-5,9-dione
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Indication
In total 1 Indication(s)
Solid tumour/cancer [ICD-11: 2A00-2F9Z]
Discontinued in Phase 3
[1]
Structure
Target Tubulin (TUB) NOUNIPROTAC [1]
Click to Show/Hide the Molecular Information and External Link(s) of This Drug
Formula
C27H41NO6S
IsoSMILES
C[C@H]1CCC[C@@]2([C@@H](O2)C[C@H](OC(=O)C[C@@H](C(C(=O)[C@@H]([C@H]1O)C)(C)C)O)/C(=C/C3=CSC(=N3)C)/C)C
InChI
1S/C27H41NO6S/c1-15-9-8-10-27(7)22(34-27)12-20(16(2)11-19-14-35-18(4)28-19)33-23(30)13-21(29)26(5,6)25(32)17(3)24(15)31/h11,14-15,17,20-22,24,29,31H,8-10,12-13H2,1-7H3/b16-11+/t15-,17+,20-,21-,22-,24-,27+/m0/s1
InChIKey
QXRSDHAAWVKZLJ-PVYNADRNSA-N
PubChem CID
448013
ChEBI ID
CHEBI:31550
TTD Drug ID
D0CV7Z
INTEDE ID
DR1795
DrugBank ID
DB03010
Type(s) of Resistant Mechanism of This Drug
  RTDM: Regulation by the Disease Microenvironment
  UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Their Corresponding Diseases
ICD-02: Benign/in-situ/malignant neoplasm
Click to Show/Hide the Resistance Disease of This Class
Endometrial cancer [ICD-11: 2C76]
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Drug Sensitivity Data Categorized by Their Corresponding Mechanisms
       Regulation by the Disease Microenvironment (RTDM) Click to Show/Hide
Key Molecule: hsa-mir-200c [1]
Molecule Alteration Expression
Up-regulation
Sensitive Disease Endometrial cancer [ICD-11: 2C76.1]
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell migration Inhibition hsa04670
In Vitro Model Hec50 cells Endometrium Homo sapiens (Human) CVCL_2929
Experiment for
Molecule Alteration
RT-PCR
Experiment for
Drug Resistance
ELISA assay
Mechanism Description Low or absent miR-200c results in aberrant expression of ZEB1 and consequent repression of E-cadherin. Reinstatement of miR-200c to such cells restores E-cadherin and dramatically reduces migration and invasion. One such gene, class IIIbeta-tubulin (TUBB3), which encodes a tubulin isotype normally found only in neuronal cells, is a direct target of miR-200c. Restoration of miR-200c increases sensitivity to microtubule-targeting agents by up to 85%. Since expression of TUBB3 is a common mechanism of resistance to microtubule-binding chemotherapeutic agents in many types of solid tumors, the ability of miR-200c to restore chemosensitivity to such agents may be explained by its ability to reduce TUBB3.
Key Molecule: BDNF/NT-3 growth factors receptor (NTRK2) [1]
Molecule Alteration Expression
Down-regulation
Sensitive Disease Endometrial cancer [ICD-11: 2C76.1]
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell migration Inhibition hsa04670
In Vitro Model Hec50 cells Endometrium Homo sapiens (Human) CVCL_2929
Experiment for
Molecule Alteration
Immunoblotting analysis
Experiment for
Drug Resistance
ELISA assay
Mechanism Description Low or absent miR-200c results in aberrant expression of ZEB1 and consequent repression of E-cadherin. Reinstatement of miR-200c to such cells restores E-cadherin and dramatically reduces migration and invasion. One such gene, class IIIbeta-tubulin (TUBB3), which encodes a tubulin isotype normally found only in neuronal cells, is a direct target of miR-200c. Restoration of miR-200c increases sensitivity to microtubule-targeting agents by up to 85%. Since expression of TUBB3 is a common mechanism of resistance to microtubule-binding chemotherapeutic agents in many types of solid tumors, the ability of miR-200c to restore chemosensitivity to such agents may be explained by its ability to reduce TUBB3.
Key Molecule: Protein quaking (QKI) [1]
Molecule Alteration Expression
Down-regulation
Sensitive Disease Endometrial cancer [ICD-11: 2C76.1]
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell migration Inhibition hsa04670
In Vitro Model Hec50 cells Endometrium Homo sapiens (Human) CVCL_2929
Experiment for
Molecule Alteration
Immunoblotting analysis
Experiment for
Drug Resistance
ELISA assay
Mechanism Description Low or absent miR-200c results in aberrant expression of ZEB1 and consequent repression of E-cadherin. Reinstatement of miR-200c to such cells restores E-cadherin and dramatically reduces migration and invasion. One such gene, class IIIbeta-tubulin (TUBB3), which encodes a tubulin isotype normally found only in neuronal cells, is a direct target of miR-200c. Restoration of miR-200c increases sensitivity to microtubule-targeting agents by up to 85%. Since expression of TUBB3 is a common mechanism of resistance to microtubule-binding chemotherapeutic agents in many types of solid tumors, the ability of miR-200c to restore chemosensitivity to such agents may be explained by its ability to reduce TUBB3.
Key Molecule: Zinc finger E-box-binding homeobox 1 (ZEB1) [1]
Molecule Alteration Expression
Down-regulation
Sensitive Disease Endometrial cancer [ICD-11: 2C76.1]
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell migration Inhibition hsa04670
In Vitro Model Hec50 cells Endometrium Homo sapiens (Human) CVCL_2929
Experiment for
Molecule Alteration
Immunoblotting analysis
Experiment for
Drug Resistance
ELISA assay
Mechanism Description Low or absent miR-200c results in aberrant expression of ZEB1 and consequent repression of E-cadherin. Reinstatement of miR-200c to such cells restores E-cadherin and dramatically reduces migration and invasion. One such gene, class IIIbeta-tubulin (TUBB3), which encodes a tubulin isotype normally found only in neuronal cells, is a direct target of miR-200c. Restoration of miR-200c increases sensitivity to microtubule-targeting agents by up to 85%. Since expression of TUBB3 is a common mechanism of resistance to microtubule-binding chemotherapeutic agents in many types of solid tumors, the ability of miR-200c to restore chemosensitivity to such agents may be explained by its ability to reduce TUBB3.
Key Molecule: Zinc finger E-box-binding homeobox 2 (ZEB2) [1]
Molecule Alteration Expression
Down-regulation
Sensitive Disease Endometrial cancer [ICD-11: 2C76.1]
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell migration Inhibition hsa04670
In Vitro Model Hec50 cells Endometrium Homo sapiens (Human) CVCL_2929
Experiment for
Molecule Alteration
Immunoblotting analysis
Experiment for
Drug Resistance
ELISA assay
Mechanism Description Low or absent miR-200c results in aberrant expression of ZEB1 and consequent repression of E-cadherin. Reinstatement of miR-200c to such cells restores E-cadherin and dramatically reduces migration and invasion. One such gene, class IIIbeta-tubulin (TUBB3), which encodes a tubulin isotype normally found only in neuronal cells, is a direct target of miR-200c. Restoration of miR-200c increases sensitivity to microtubule-targeting agents by up to 85%. Since expression of TUBB3 is a common mechanism of resistance to microtubule-binding chemotherapeutic agents in many types of solid tumors, the ability of miR-200c to restore chemosensitivity to such agents may be explained by its ability to reduce TUBB3.
       Unusual Activation of Pro-survival Pathway (UAPP) Click to Show/Hide
Key Molecule: Fibronectin (FN1) [1]
Molecule Alteration Expression
Down-regulation
Sensitive Disease Endometrial cancer [ICD-11: 2C76.1]
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell migration Inhibition hsa04670
In Vitro Model Hec50 cells Endometrium Homo sapiens (Human) CVCL_2929
Experiment for
Molecule Alteration
Immunoblotting analysis
Experiment for
Drug Resistance
ELISA assay
Mechanism Description Low or absent miR-200c results in aberrant expression of ZEB1 and consequent repression of E-cadherin. Reinstatement of miR-200c to such cells restores E-cadherin and dramatically reduces migration and invasion. One such gene, class IIIbeta-tubulin (TUBB3), which encodes a tubulin isotype normally found only in neuronal cells, is a direct target of miR-200c. Restoration of miR-200c increases sensitivity to microtubule-targeting agents by up to 85%. Since expression of TUBB3 is a common mechanism of resistance to microtubule-binding chemotherapeutic agents in many types of solid tumors, the ability of miR-200c to restore chemosensitivity to such agents may be explained by its ability to reduce TUBB3.
Key Molecule: Tubulin beta-3 chain (TUBB3) [1]
Molecule Alteration Expression
Down-regulation
Sensitive Disease Endometrial cancer [ICD-11: 2C76.1]
Experimental Note Revealed Based on the Cell Line Data
Cell Pathway Regulation Cell migration Inhibition hsa04670
In Vitro Model Hec50 cells Endometrium Homo sapiens (Human) CVCL_2929
Experiment for
Molecule Alteration
Immunoblotting analysis
Experiment for
Drug Resistance
ELISA assay
Mechanism Description Low or absent miR-200c results in aberrant expression of ZEB1 and consequent repression of E-cadherin. Reinstatement of miR-200c to such cells restores E-cadherin and dramatically reduces migration and invasion. One such gene, class IIIbeta-tubulin (TUBB3), which encodes a tubulin isotype normally found only in neuronal cells, is a direct target of miR-200c. Restoration of miR-200c increases sensitivity to microtubule-targeting agents by up to 85%. Since expression of TUBB3 is a common mechanism of resistance to microtubule-binding chemotherapeutic agents in many types of solid tumors, the ability of miR-200c to restore chemosensitivity to such agents may be explained by its ability to reduce TUBB3.
References
Ref 1 MicroRNA-200c mitigates invasiveness and restores sensitivity to microtubule-targeting chemotherapeutic agents. Mol Cancer Ther. 2009 May;8(5):1055-66. doi: 10.1158/1535-7163.MCT-08-1046. Epub 2009 May 12.

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