mk2

MK2-IN-3 hydrate (MK-2 Inhibitor III) is an orally active, selective, and ATP-competitive inhibitor of MAPKAP-K2 (MK-2) (IC50 of 0.85 nM)

MK2-IN-1 hydrochloride (MK 25) is a highly selective, non-ATP competitive inhibitor of p38/mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2 or MK2, IC50: 0.11 μM) [1].

CMPD1 is a non-ATP-competitive p38 MAPK-mediated MK2 phosphorylation inhibitor(apparent Ki (Kiapp): 330 nM).

PF-3644022 is an effective, selective, and ATP-competitive MAPKAPK2 (MK2) inhibitor (IC50: 5.2 nM and a Ki of 3 nM). PF-3644022 potently inhibits TNFα production and has an anti-inflammatory effect. PF-3644022 also inhibits MK3 and p38 regulated/activated

Zunsemetinib (ATI-450) is an orally active and selective inhibitor of the p38α mitogen-activated protein kinase-activated protein kinase 2 (MK2) pathway.Zunsemetinib is used to study spondyloarthritis and rheumatoid arthritis.

MK2-IN-3 (MK2 Inhibitor III) is a potent, cell-permeable inhibitor of mitogen-activated protein kinase-activated protein kinase 2 (MAPKAP-K2 or MK-2) and can be used for the treatment of rheumatoid arthritis

p38α-MK2-IN-1 (Compound 36) is an inhibitor of the p38α-MK2 complex, with an IC50 of 5 nM. This compound exhibits significant anti-inflammatory properties and has the ability to aid in joint repair.

MK2-IN-7 (Compound 144) is an inhibitor of mitogen-activated protein kinase-activated protein kinase-2 (MK2). It shows potential for research in inflammatory diseases, autoimmune disorders, and cancer.

MK2-IN-1 is a potent and selecitve MAPKAPK2(MK2) inhibitor(IC50=0.11 uM) with a non-ATP competitive binding mode.

MK2-IN-4, a MAPKAPK2 (MK2) inhibitor with an IC50 of 45 nM, can be used in cancer, inflammation, and immunology studies.

MK2-IN-5, a pseudosubstrate of Mk2 with an inhibition constant (K_i) of 8 μM, selectively targets the protein interaction domain of the MAPK pathway and inhibits the phosphorylation of HSP25 and HSP27 [1] [2] [3].

MK2-IN-6 (Compound 11) is an effective and selective irreversible inhibitor of MK2 with an IC50 value of 2.3 nM. It suppresses the kinase activity of MK2, leading to sustained inhibition of MK2 signaling and reduction of pathological inflammatory factors in macrophages. MK2-IN-6 is capable of inhibiting the M2-like protein phenotype in macrophages both in vitro and in vivo, showing potential for use in colorectal cancer research.

Adenosine 5'-methylenediphosphate (sodium salt) is also referred to as an inhibitor of ecto-5'-nucleotidase.

MK256 is a novel CDK8 inhibitor that demonstrates potent antitumor activity against AML by inhibiting the STAT pathway. It induces differentiation and maturation while inhibiting proliferation in AML cell lines. MK256 decreases the phosphorylation of STAT1(S727) and STAT5(S726) and reduces mRNA expression of MCL-1 and CCL2 in these cells. Its efficacy is validated in the MOLM-14 xenograft model, showing phosphorylation inhibition of STAT1(S727) and STAT5(S726) post-treatment. Pharmacokinetic studies in the MOLM-14 model reveal a dose-dependent inhibition of the STAT pathway. Both in vitro and in vivo studies confirm that MK256 effectively downregulates the STAT pathway.

MK204 is an inhibitor of AKR1B10, a tumor marker and promising antineoplastic target.

UR-MK299 is a NPY Y1 receptor antagonist.

AMK218 (Immobilized amoxicillin acylase) serves as a biocatalyst and is a key enzyme in new biocatalyst technologies. Enzyme engineering focuses on improving enzyme reaction kinetics, substrate selectivity, and activity under extreme conditions (e.g., low or high pH). Modifications that introduce stimulus responsiveness enable dynamic control of their activity.

Ferrostatin-1 (Fer-1) is a potent and selective inhibitor of iron death. Ferrostatin-1 potently inhibits Erastin-induced iron death in HT-1080 cells with an EC50 of 60 nM. Ferrostatin-1 also exhibits antioxidant and antifungal activities.

Ralimetinib is a selective inhibitor that blocks phosphorylation of MK2 at Thr334, without affecting the phosphorylation of p38α MAPK, JNK, ERK1/2, c-Jun, ATF2, or c-Myc. Ralimetinib functions as an ATP-competitive inhibitor of p38 MAPK α/β, demonstrating IC50 values of 5.3 and 3.2 nM, respectively, and is under investigation as an anti-inflammatory and anticancer therapeutic.

Tpl2 Kinase Inhibitor 1 is an effective and selective Tpl2 inhibitor.

Antitrypanosomal agent 23 is an antiparasitic compound effective against intracellular amastigotes of Trypanosoma cruzi in LLC-MK2 and C2C12 cells, demonstrating activity with IC50 values of 0.10 and 0.11 μM, respectively. It also acts as a weak inhibitor of recombinant Trypanosoma cruzi sialyltransferase (TcTS) with an IC50 of 1.1 mM.

(R)-STU104-d6 is a deuterium-labeled variant of (R)-STU104. This compound acts as a potent and orally active inhibitor of the interaction between TAK1 and MKK3 proteins, exhibiting IC50 values of 0.58 μM for TNF-α and 4.0 μM for MKK3 phosphorylation. By binding to MKK3, (R)-STU104 hinders TAK1's ability to phosphorylate MKK3, thereby disrupting the TAK1/MKK3/p38/MnK1/MK2/elF4E signaling pathway. It is utilized in research related to ulcerative colitis.

Tpl2 kinase inhibitor is an inhibitor of tumor progression locus 2 (Tpl2; IC50= 0.05 μM).1It is selective for Tpl2 over MEK, p38 MAPK, Src, MK2, and PKC (IC50s = >40, 180, >400, 110, and >400 μM, respectively). Tpl2 kinase inhibitor inhibits LPS-induced TNF-α production in isolated human monocytes and whole blood (IC50s = 0.7 and 8.5 μM, respectively). It enhances differentiation induced by calcitriol in HL-60 and U937 leukemia cells when used at a concentration of 5 μM.2Tpl2 kinase inhibitor (5 μM) inhibits the proliferation of KG-1a leukemia cells.3 1.Garvin, L.K., Green, N., Hu, Y., et al.Inhibition of Tpl2 kinase and TNF-α production with 1,7-naphthyridine-3-carbonitriles: Synthesis and structure-activity relationshipsBioor. Med. Chem. Lett.15(23)5288-5292(2005) 2.Wang, X., and Studzinski, G.P.Expression of MAP3 kinase COT1 is up-regulated by 1,25-dihydroxyvitamin D3 in parallel with activated c-jun during differentiation of human myeloid leukemia cellsJ. Steroid. Biochem. Mol. Biol.121(1-2)395-398(2010) 3.Wang, X., Gocek, E., Novik, V., et al.Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D3Cell Cycle9(22)4542-4551(2010)

Potent and selective p38α and p38β degrader (DC50 < 50 nM). Displays no significant degradation of p38γ, p38δ, JNK1/2 or ERK1/2. Inhibits phosphorylation of MK2 in UV-treated cancer cells and LPS-stimulated bone marrow-derived macrophages (BMDM). Exhibits similar effect to p38α gene knockout in BBL358 cells. Active in vivo.