General Information of the Drug (ID: M6APDG01933)
Name
PD-0166326
Synonyms
PD-166326
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Status
Investigative
Structure
Formula
C21H16Cl2N4O2
InChI
1S/C21H16Cl2N4O2/c1-27-19-13(9-15(20(27)29)18-16(22)6-3-7-17(18)23)10-24-21(26-19)25-14-5-2-4-12(8-14)11-28/h2-10,28H,11H2,1H3,(H,24,25,26)
InChIKey
ZIQFYVPVJZEOFS-UHFFFAOYSA-N
PubChem CID
447700
TTD Drug ID
D0P3JW
Target Gene(s) and Their Upstream m6A Regulator, Together with the Effect of Target Gene(s) in Drug Response
The target genes involved in drug-target interaction (such as drug-metabolizing enzymes, drug transporters and therapeutic targets) and drug-mediated cell death signaling (including modulating DNA damage and repair capacity, escaping from drug-induced apoptosis, autophagy, cellular metabolic reprogramming, oncogenic bypass signaling, cell microenvironment, cell stemness, etc.) could be regulated by m6A regulator(s) and affected their corresponding drug response. You can browse detailed information on drug-related target gene(s) mediated by m6A regulators.
Epidermal growth factor receptor (EGFR)
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
Response Summary Epidermal growth factor receptor (EGFR) is a therapeutic target for PD-0166326. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of PD-0166326 through regulating the expression of Epidermal growth factor receptor (EGFR). [1], [2]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Epidermal growth factor receptor (EGFR) is a therapeutic target for PD-0166326. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of PD-0166326 through regulating the expression of Epidermal growth factor receptor (EGFR). [2], [3]
RNA demethylase ALKBH5 (ALKBH5)
In total 1 mechanisms lead to this potential drug response
Response Summary Epidermal growth factor receptor (EGFR) is a therapeutic target for PD-0166326. The RNA demethylase ALKBH5 (ALKBH5) has potential in affecting the response of PD-0166326 through regulating the expression of Epidermal growth factor receptor (EGFR). [2], [4]
YTH domain-containing family protein 1 (YTHDF1)
In total 1 mechanisms lead to this potential drug response
Response Summary Epidermal growth factor receptor (EGFR) is a therapeutic target for PD-0166326. The YTH domain-containing family protein 1 (YTHDF1) has potential in affecting the response of PD-0166326 through regulating the expression of Epidermal growth factor receptor (EGFR). [2], [5]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
Response Summary Epidermal growth factor receptor (EGFR) is a therapeutic target for PD-0166326. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of PD-0166326 through regulating the expression of Epidermal growth factor receptor (EGFR). [2], [6]
YTH domain-containing family protein 3 (YTHDF3)
In total 1 mechanisms lead to this potential drug response
Response Summary Epidermal growth factor receptor (EGFR) is a therapeutic target for PD-0166326. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of PD-0166326 through regulating the expression of Epidermal growth factor receptor (EGFR). [2], [7]
Platelet-derived growth factor receptor alpha (PDGFRA)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Platelet-derived growth factor receptor alpha (PDGFRA) is a therapeutic target for PD-0166326. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of PD-0166326 through regulating the expression of Platelet-derived growth factor receptor alpha (PDGFRA). [2], [8]
Platelet-derived growth factor receptor beta (PDGFRB)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
Response Summary Platelet-derived growth factor receptor beta (PDGFRB) is a therapeutic target for PD-0166326. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of PD-0166326 through regulating the expression of Platelet-derived growth factor receptor beta (PDGFRB). [2], [9]
Stress-activated protein kinase 2a (p38 alpha)
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2)
In total 1 mechanisms lead to this potential drug response
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for PD-0166326. The Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has potential in affecting the response of PD-0166326 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [10], [11]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for PD-0166326. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of PD-0166326 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [11], [12]
YTH domain-containing family protein 3 (YTHDF3)
In total 1 mechanisms lead to this potential drug response
Response Summary Stress-activated protein kinase 2a (p38 alpha) is a therapeutic target for PD-0166326. The YTH domain-containing family protein 3 (YTHDF3) has potential in affecting the response of PD-0166326 through regulating the expression of Stress-activated protein kinase 2a (p38 alpha). [10], [11]
References
Ref 1 METTL14 Inhibits Hepatocellular Carcinoma Metastasis Through Regulating EGFR/PI3K/AKT Signaling Pathway in an m6A-Dependent Manner. Cancer Manag Res. 2020 Dec 23;12:13173-13184. doi: 10.2147/CMAR.S286275. eCollection 2020.
Ref 2 Biochemical and cellular effects of c-Src kinase-selective pyrido[2, 3-d]pyrimidine tyrosine kinase inhibitors. Biochem Pharmacol. 2000 Oct 1;60(7):885-98. doi: 10.1016/s0006-2952(00)00405-6.
Ref 3 METTL3 induces PLX4032 resistance in melanoma by promoting m(6)A-dependent EGFR translation. Cancer Lett. 2021 Dec 1;522:44-56. doi: 10.1016/j.canlet.2021.09.015. Epub 2021 Sep 13.
Ref 4 ALKBH5 inhibited autophagy of epithelial ovarian cancer through miR-7 and BCL-2. J Exp Clin Cancer Res. 2019 Apr 15;38(1):163. doi: 10.1186/s13046-019-1159-2.
Ref 5 Insufficient Radiofrequency Ablation Promotes Hepatocellular Carcinoma Metastasis Through N6-Methyladenosine mRNA Methylation-Dependent Mechanism. Hepatology. 2021 Sep;74(3):1339-1356. doi: 10.1002/hep.31766.
Ref 6 YTHDF2 suppresses cell proliferation and growth via destabilizing the EGFR mRNA in hepatocellular carcinoma. Cancer Lett. 2019 Feb 1;442:252-261. doi: 10.1016/j.canlet.2018.11.006. Epub 2018 Nov 10.
Ref 7 YTHDF3 Induces the Translation of m(6)A-Enriched Gene Transcripts to Promote Breast Cancer Brain Metastasis. Cancer Cell. 2020 Dec 14;38(6):857-871.e7. doi: 10.1016/j.ccell.2020.10.004. Epub 2020 Oct 29.
Ref 8 METTL3-mediated N (6)-methyladenosine modification governs pericyte dysfunction during diabetes-induced retinal vascular complication. Theranostics. 2022 Jan 1;12(1):277-289. doi: 10.7150/thno.63441. eCollection 2022.
Ref 9 Mutant NPM1-Regulated FTO-Mediated m(6)A Demethylation Promotes Leukemic Cell Survival via PDGFRB/ERK Signaling Axis. Front Oncol. 2022 Feb 8;12:817584. doi: 10.3389/fonc.2022.817584. eCollection 2022.
Ref 10 N6-methyladenosine reader YTH N6-methyladenosine RNA binding protein 3 or insulin like growth factor 2 mRNA binding protein 2 knockdown protects human bronchial epithelial cells from hypoxia/reoxygenation injury by inactivating p38 MAPK, AKT, ERK1/2, and NF-KappaB pathways. Bioengineered. 2022 May;13(5):11973-11986. doi: 10.1080/21655979.2021.1999550.
Ref 11 Structure-activity relationships of 6-(2,6-dichlorophenyl)-8-methyl-2-(phenylamino)pyrido[2,3-d]pyrimidin-7-ones: toward selective Abl inhibitors. Bioorg Med Chem Lett. 2009 Dec 15;19(24):6872-6. doi: 10.1016/j.bmcl.2009.10.085. Epub 2009 Oct 23.
Ref 12 m(6)A methyltransferase METTL3 suppresses colorectal cancer proliferation and migration through p38/ERK pathways. Onco Targets Ther. 2019 Jun 4;12:4391-4402. doi: 10.2147/OTT.S201052. eCollection 2019.