n-myristoyltransferase

DDD100097 is a potent N-myristoyltransferase inhibitor with potential inhibitory effects on Trypanosoma brucei, which can be used to study neurological disorders.

DDD85646 is an inhibitor of T. brucei N-myristoyltransferase with a Ki of 1.44 nM, an IC50 of 2 nM and an EC50 of 2 nM. The IC50 of hNMT is 4 nM.

NMT-IN-7 is an inhibitor of N-myristoyltransferase (NMT) with an IC50 of 2.1 nM for HsNMT1M and demonstrates toxicity with an IC50 of 0.6 nM against SU-DHL-10 cells. It can be utilized as an ADC cytotoxin.

CpNMT-IN-1 (Compound 11e) is an inhibitor of N-myristoyltransferase (CpNMT) with an IC50 value of 2.5 μM. It also inhibits the growth of microsporidia, demonstrating an EC50 value of 6.9 μM.

tris(dibenzylideneacetone)dipalladium (Tris DBA) is a N-myristoyltransferase-1 (NMT-1) inhibitor

RO-09-4609 is a potent and selective inhibitor of Candida albicans N-myristoyltransferase (CaNmt).

SC-58272 is an inhibitor of N-myristoyltransferase (Nmt), a target for anti-fungal and anti-viral therapy.

Myristoyl coenzyme A (myristoyl-CoA) is a derivative of CoA that contains the long-chain fatty acid myristic acid . It is a substrate for N-myristoyltransferase during myristoylation, a process that adds a myristoyl group to proteins either during translation to modify protein activity or post-translationally in apoptotic cells. It is also a substrate in the de novo synthesis of phosphatidylinositol .

PCLX-001 is a small-molecule compound that acts as an orally active inhibitor of N-myristoyltransferase (NMT), specifically targeting NMT1 and NMT2 with IC50 values of 5 nM and 8 nM, respectively. This compound demonstrates anti-tumor effects and effectively inhibits the early signaling of B-cell receptor (BCR). Consequently, PCLX-001 is a valuable tool for researching B-cell malignancies [1] [2].

FTR1335 is a CaNMT inhibitor (IC50 = 0.49 nM) with good fungal selectivity. CaNMT inhibitors are fungicidal and show antifungal activity against Candida (especially fluconazole-resistant strains). They function by inhibiting N-myristoyltransferase (NMT), which catalyzes the transfer of a C14 fatty acif from myristoyl-CoA to the N-terminal of glycine in many fungal proteins. Without this process, fungi can die. This process also occurs in humans, and as such selectivity is an important characteristic of these drugs.

PF00349412 is a selective inhibitor of protozoan protein N-myristoyltransferases. Inhibition of N-myristoyltransferase has been validated pre-clin. as a target for the treatment of fungal and trypanosome infections, using species-specific inhibitors.

Myristoyl coenzyme A lithium, a compound marked by lithium in its myristoylated form, plays a crucial role in the biochemical mechanism of myristoylation, essential for both viral functionalities and tumor growth in colon epithelial cells. This process is predominantly governed by N-myristoyltransferase (NMT), which exhibits increased activity in colon epithelial tumors compared to normal cells. The activity of NMT is significantly influenced by the reduction of coenzyme A (CoA), a vital regulator that enhances NMT's ability to induce myristoylation, unlike its oxidized form which impedes this process. Consequently, Myristoyl coenzyme A serves as an inhibitor to the demyristoylation activity, showcasing its potential as an anticancer and antiviral agent.

MYX1715 is an inhibitor of N-myristoyltransferase (NMT), exhibiting a KD of 0.09 nM. It inhibits the proliferation of LU0884 and LU2511, with IC50 values of 44 nM and 9 nM, respectively. In mouse models, MYX1715 demonstrates antitumor activity against neuroblastoma and gastric cancer. Additionally, MYX1715 can be utilized as a toxin in ADCs.

18-Azido-stearic acid is a click chemistry reagent containing an azido group. It serves as a hydrophobic bioconjugation linker (utilizing N-myristoyltransferase) and can be further modified at the azido position through click chemistry.

IMP-1088 is a potent inhibitor of human N-myristoyltransferases NMT1 and NMT2 dual.

Myristoyl coenzyme A lithium is a myristoylated form of coenzyme A (CoA). Myristoylation, an essential process in viruses, is typically regulated by N-myristoyltransferase (NMT), which is more active in colon epithelial tumors than in normal cells. The reduced form of coenzyme A (CoA) is a key regulator of NMT activity, whereas the oxidized form does not permit NMT to promote myristoylation. Myristoyl coenzyme A potentially inhibits demyristoylation, suggesting anticancer and antiviral mechanisms.