General Information of the Drug (ID: M6APDG03324)
Name
BNP-1350
Synonyms
Cositecan; Cositecan (USAN); Cositecan [USAN:INN]; Karenitecin; Karenitecin (TN); POADTFBBIXOWFJ-VWLOTQADSA-N; SCHEMBL2315201; Z-3161; ZINC169746728; 1H-Pyrano(3',4':6,7)indolizino(1,2-b)quinoline-3,14(4H,12H)-dione, 4-ethyl-4-hydroxy-11-(2-trimethylsilyl)ethyl)-, (4S)-; 203923-89-1; 24R60NVC41; 7-Trimethylsilylethylcamptothecin; 923K891; AC1L3WN8; AN-29989; BNP 1350; BNP-1350; BNP1350; CHEMBL1997373; CS-0003573; D09327; DB 172; DB05806; DTXSID90174340; HY-14812; NCI60_038797; NSC-710270; NSC710270; UNII-24R60NVC41
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Status
Phase 3
Structure
Formula
C25H28N2O4Si
InChI
1S/C25H28N2O4Si/c1-5-25(30)19-12-21-22-17(13-27(21)23(28)18(19)14-31-24(25)29)15(10-11-32(2,3)4)16-8-6-7-9-20(16)26-22/h6-9,12,30H,5,10-11,13-14H2,1-4H3/t25-/m0/s1
InChIKey
POADTFBBIXOWFJ-VWLOTQADSA-N
PubChem CID
148202
VARIDT Drug ID
DR01349
INTEDE Drug ID
DR1901
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.
Breast cancer resistance protein (ABCG2)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Breast cancer resistance protein (ABCG2) is a therapeutic target for BNP-1350. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of BNP-1350 through regulating the expression of Breast cancer resistance protein (ABCG2). [1], [2]
Cytochrome P450 2C8 (CYP2C8)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
Response Summary Cytochrome P450 2C8 (CYP2C8) is a therapeutic target for BNP-1350. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of BNP-1350 through regulating the expression of Cytochrome P450 2C8 (CYP2C8). [3], [4]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
Response Summary Cytochrome P450 2C8 (CYP2C8) is a therapeutic target for BNP-1350. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of BNP-1350 through regulating the expression of Cytochrome P450 2C8 (CYP2C8). [3], [4]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Cytochrome P450 2C8 (CYP2C8) is a therapeutic target for BNP-1350. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of BNP-1350 through regulating the expression of Cytochrome P450 2C8 (CYP2C8). [3], [4]
YTH domain-containing protein 2 (YTHDC2)
In total 1 mechanisms lead to this potential drug response
Response Summary Cytochrome P450 2C8 (CYP2C8) is a therapeutic target for BNP-1350. The YTH domain-containing protein 2 (YTHDC2) has potential in affecting the response of BNP-1350 through regulating the expression of Cytochrome P450 2C8 (CYP2C8). [3], [4]
References
Ref 1 METTL3 promotes adriamycin resistance in MCF-7 breast cancer cells by accelerating pri-microRNA-221-3p maturation in a m6A-dependent manner. Exp Mol Med. 2021 Jan;53(1):91-102. doi: 10.1038/s12276-020-00510-w. Epub 2021 Jan 8.
Ref 2 Pharmacogenomic importance of ABCG2. Pharmacogenomics. 2008 Aug;9(8):1005-9.
Ref 3 Methylation of adenosine at the N(6) position post-transcriptionally regulates hepatic P450s expression. Biochem Pharmacol. 2020 Jan;171:113697. doi: 10.1016/j.bcp.2019.113697. Epub 2019 Nov 7.
Ref 4 Evaluation of in vitro drug interactions with karenitecin, a novel, highly lipophilic camptothecin derivative in phase II clinical development. J Clin Pharmacol. 2003 Sep;43(9):1008-14. doi: 10.1177/0091270003255921.