General Information of the Drug (ID: M6APDG01231)
Name
EMD-1204831
Status
Phase 1
Structure
Formula
C25H27N7O3
InChI
1S/C25H27N7O3/c1-30-18-21(14-28-30)23-5-6-24(33)32(29-23)17-19-3-2-4-20(13-19)25-26-15-22(16-27-25)35-12-9-31-7-10-34-11-8-31/h2-6,13-16,18H,7-12,17H2,1H3
InChIKey
CIUKPBWULKEZMF-UHFFFAOYSA-N
PubChem CID
25134692
TTD Drug ID
D0Y8UV
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.
Proto-oncogene c-Met (MET)
Methyltransferase-like 3 (METTL3)
In total 1 mechanisms lead to this potential drug response
Response Summary Proto-oncogene c-Met (MET) is a therapeutic target for EMD-1204831. The Methyltransferase-like 3 (METTL3) has potential in affecting the response of EMD-1204831 through regulating the expression of Proto-oncogene c-Met (MET). [1], [2]
References
Ref 1 RNA m(6) A methylation regulates uveal melanoma cell proliferation, migration, and invasion by targeting c-Met. J Cell Physiol. 2020 Oct;235(10):7107-7119. doi: 10.1002/jcp.29608. Epub 2020 Feb 4.
Ref 2 E7050: a dual c-Met and VEGFR-2 tyrosine kinase inhibitor promotes tumor regression and prolongs survival in mouse xenograft models. Cancer Sci. 2010 Jan;101(1):210-5. doi: 10.1111/j.1349-7006.2009.01343.x. Epub 2009 Sep 2.