Scientific Reviews
Product Guides
Blogs
Topics
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
77 Results for "
RNA modification
" in MedChemExpress (MCE) Product Catalog:
Products (77)
77 Results for "RNA modification" in MCE Product Catalog:
8
8 Publications Verification
Synonyms: 6-Methyladenosine; N-Methyladenosine
Target:
4
4 Cited Publications
Category:
Alkaloids Microorganisms Immune System Disorder Other Diseases Disease markers Endogenous metabolite Disease Research Fields Cancer
Target:
4
Category:
Natural Products Other disease Disease markers Endogenous metabolite Disease Research Fields Cancer
Target:
3
Category:
Natural Products Microorganisms Other Diseases Endogenous metabolite Disease Research Fields
Target:
3
3 Cited Publications
Cat. No.: HY-W037893
CAS No.: 122323-88-0
Synonyms: Methyl piperazine-2-carboxylate dihydrochloride; METTL3 activator-1
Research Areas:
CHMA1004 (Methyl piperazine-2-carboxylate; METTL3 activator-1) dihydrochloride is a METTL3/METTL14/WTAP methyltransferase complex activator. CHMA1004 dihydrochloride exhibits neuroprotective and anxiolytic potential by enhancing m 6A methylation modification of RNA. CHMA1004 dihydrochloride promotes HIV replication in an infection context. CHMA1004 dihydrochloride can be used in studies related to anxiety disorders and HIV-1 infection .
3
3 Cited Publications
Cat. No.: HY-P1291
CAS No.: 201422-03-9
Target:
Research Areas:
3
3 Cited Publications
Cat. No.: HY-P1291A
Target:
Research Areas:
2
2 Cited Publications
2
2 Cited Publications
Cat. No.: HY-W008091
CAS No.: 554-01-8
2
2 Cited Publications
Cat. No.: HY-162080
CAS No.: 374705-10-9
Target:
Research Areas:
METTL1-WDR4-IN-1 (Compound 1) is a selective competitive inhibitor of the methyltransferase complex METTL1-WDR4 (IC50 = 144 μM). METTL1-WDR4-IN-1 inhibits the m 7G methyltransferase activity of the METTL1-WDR4 complex, blocking m 7G modification of PKM mRNA, reducing PKM2 protein expression, disrupting the METTL1/PKM2/H3K9la positive feedback loop, and simultaneously inhibiting PKM2 nuclear translocation-mediated CD155 transcriptional activation. METTL1-WDR4-IN-1 can inhibit tumor cell proliferation, weaken glycolytic metabolism, reverse tumor immune evasion (restoring NK cell and CD8 + T cell function), and regulate RNA epigenetic modification and the tumor immune microenvironment. METTL1-WDR4-IN-1 can be used in immunotherapy research for cancers such as colorectal cancer, and is particularly suitable for use in combination with PKM2 inhibitors to enhance anti-tumor treatment efficacy .
2
2 Cited Publications
Synonyms: 6-Methyladenosine (Standard); N-Methyladenosine (Standard)
2
2 Cited Publications
Cat. No.: HY-W008091R
CAS No.: 554-01-8
2
2 Cited Publications
Cat. No.: HY-W008091A
CAS No.: 58366-64-6
Research Areas:
5-Methylcytosine hydrochloride is a well-characterized DNA modification in prokaryotes and eukaryotes. 5-Methylcytosine hydrochloride forms symmetrical methylation on CpG dinucleotides in DNA, stabilizes tRNA/rRNA structure in RNA, and affects mRNA translation. 5-Methylcytosine hydrochloride can be oxidized to generate 5hmC, 5fC, and 5caC. 5-Methylcytosine hydrochloride can be used in epigenetics, developmental biology, and the study of diseases such as colorectal cancer and hepatocellular carcinoma .
2
2 Cited Publications
Cat. No.: HY-122524A
CAS No.: 81100-62-1
Research Areas:
7-Methylguanosine iodide is an iodide of 7-Methylguanosine (HY-122524). 7-Methylguanosine is a modified nucleoside widely present in various RNAs and a key metabolite of the 5'-cap structure of eukaryotic mRNA. 7-Methylguanosine plays important roles in stabilizing RNA structures, regulating translation, and other aspects .
2
2 Cited Publications
Cat. No.: HY-162080A
Target:
Research Areas:
METTL1-WDR4-IN-1 (Compound 1) TFA is a selective competitive inhibitor of the methyltransferase complex METTL1-WDR4 (IC50=144 μM). METTL1-WDR4-IN-1 TFA inhibits the m 7G methyltransferase activity of the METTL1-WDR4 complex, blocking the m 7G modification of PKM mRNA, reducing PKM2 protein expression, disrupting the METTL1/PKM2/H3K9la positive feedback loop, and simultaneously inhibiting PKM2 nuclear translocation-mediated CD155 transcriptional activation. METTL1-WDR4-IN-1 TFA can inhibit tumor cell proliferation, weaken glycolytic metabolism, reverse tumor immune evasion (restoring NK cell and CD8 + T cell function), and regulate RNA epigenetic modification and the tumor immune microenvironment. METTL1-WDR4-IN-1 TFA can be used in immunotherapy research for cancers such as colorectal cancer, and is particularly suitable for use in combination with PKM2 inhibitors to enhance anti-tumor treatment efficacy .
1
1 Cited Publications
Research Areas:
MY-1B is a covalent inhibitor of the RNA Methyltransferase NSUN2 (IC50: 1.3 μM). MY-1B stereoselectively ligands active-site cysteine residues (C271) of NSUN2. MY-1B can stereoselectively and covalently bind to PSME1, disrupting the proteasome regulatory complex and downregulating the presentation of specific MHC-I subtypes .
1
Target:
1
1 Cited Publications
Synonyms: N3-Methyluridine
Target:
1
1 Cited Publications
Cat. No.: HY-P10387
1
1 Cited Publications
(S)-mchm5U is a hydroxylated form of mcm5U, may be present in tRNA from the silkworm Bombyx mori. (S)-mchm5U may be present also in mammalian tRNA, and that the ALKBH8 oxygenase could be responsible for its formation. (S)-mchm5U can be used for RNA modification synthesis .
-
-
Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
