m6A-centered Drug Response Information

General Information of the Drug (ID: M6APDG03149)
Name
KRP-101
Synonyms
PPAR alpha agonist (hyperlipidemia), Kyorin
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Status
Discontinued in Phase 2
Structure
Formula
C26H26FNO5
InChI
1S/C26H26FNO5/c1-3-19(26(30)31)14-18-6-13-24(32-2)23(15-18)25(29)28-16-17-4-9-21(10-5-17)33-22-11-7-20(27)8-12-22/h4-13,15,19H,3,14,16H2,1-2H3,(H,28,29)(H,30,31)/t19-/m0/s1
InChIKey
VRHOBXXCNBZJRX-IBGZPJMESA-N
PubChem CID
9825046
TTD Drug ID
D0B8JQ
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.
Peroxisome proliferator-activated receptor alpha (PPARA)
Fat mass and obesity-associated protein (FTO)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Peroxisome proliferator-activated receptor alpha (PPARA) is a therapeutic target for KRP-101. The Fat mass and obesity-associated protein (FTO) has potential in affecting the response of KRP-101 through regulating the expression of Peroxisome proliferator-activated receptor alpha (PPARA). [1], [2]
Methyltransferase-like 14 (METTL14)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Peroxisome proliferator-activated receptor alpha (PPARA) is a therapeutic target for KRP-101. The Methyltransferase-like 14 (METTL14) has potential in affecting the response of KRP-101 through regulating the expression of Peroxisome proliferator-activated receptor alpha (PPARA). [2], [3]
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Peroxisome proliferator-activated receptor alpha (PPARA) is a therapeutic target for KRP-101. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of KRP-101 through regulating the expression of Peroxisome proliferator-activated receptor alpha (PPARA). [2], [4]
Wilms tumor 1-associating protein (WTAP)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Peroxisome proliferator-activated receptor alpha (PPARA) is a therapeutic target for KRP-101. The Wilms tumor 1-associating protein (WTAP) has potential in affecting the response of KRP-101 through regulating the expression of Peroxisome proliferator-activated receptor alpha (PPARA). [2], [3]
YTH domain-containing family protein 2 (YTHDF2)
In total 1 mechanisms lead to this potential drug response
 Regulator Info 
Response Summary Peroxisome proliferator-activated receptor alpha (PPARA) is a therapeutic target for KRP-101. The YTH domain-containing family protein 2 (YTHDF2) has potential in affecting the response of KRP-101 through regulating the expression of Peroxisome proliferator-activated receptor alpha (PPARA). [2], [4]
References
Ref 1 Resveratrol Attenuates High-Fat Diet Induced Hepatic Lipid Homeostasis Disorder and Decreases m(6)A RNA Methylation. Front Pharmacol. 2020 Dec 18;11:568006. doi: 10.3389/fphar.2020.568006. eCollection 2020.
Ref 2 Cardiac function and metabolism in Type 2 diabetic mice after treatment with BM 17.0744, a novel PPAR-alpha activator. Am J Physiol Heart Circ Physiol. 2002 Sep;283(3):H949-57. doi: 10.1152/ajpheart.00226.2001.
Ref 3 A METTL3-METTL14 complex mediates mammalian nuclear RNA N6-adenosine methylation. Nat Chem Biol. 2014 Feb;10(2):93-5. doi: 10.1038/nchembio.1432. Epub 2013 Dec 6.
Ref 4 Circadian Clock Regulation of Hepatic Lipid Metabolism by Modulation of m(6)A mRNA Methylation. Cell Rep. 2018 Nov 13;25(7):1816-1828.e4. doi: 10.1016/j.celrep.2018.10.068.