p38α mapk

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.

p38αMAPK/CK1δ inhibitor-1 (Compound 3) exhibits inhibitory activity against p38αMAPK and CK1δ, with IC50 values of 0.185 µM and 0.089 µM, respectively.

p38 MAPK inhibitor is a potent inhibitor of p38 MAP kinase (IC50 = 35 nM). It inhibits senescence induced by the oncogene RAS.

p38 MAPK-IN-9 (Compound 15) is an orally active and highly selective inhibitor of the p38αMAP kinase (p38 MAPK), with an IC50 value of 9.6 nM. It holds potential for research into inflammatory diseases such as rheumatoid arthritis, septic shock, and chronic obstructive pulmonary disease.

p38 MAPK inhibitor IV is an ATP-competitive inhibitor of p38 MAP kinases with IC50 values of 0.13, 0.55, 5.47, and 8.63 μM for p38α, p38β, p38x, and p38δ, respectively, in vitro.[1] It also inhibits LPS-induced TNF-α and IL-1β cytokine production (IC50s = 22 and 44 nM, respectively) in human peripheral blood mononuclear cells.

p38 MAPK-IN-3 (Compound 2c) is a potent inhibitor of p38α MAPK, exhibiting antitumor properties through the promotion of apoptosis and the enhancement of reactive oxygen species (ROS) production [1].

p38 MAPK-IN-2 is a potent inhibitor of p38 kinase.

p38 MAPK-IN-1 is a novel selective p38 MAPK inhibitor with high potency, long duration, and low clearance, which reduces inflammatory responses by inhibiting LPS-induced TNF-α production.

p38 MAPK-IN-6 (compound c47) is an inhibitor of p38 MAPK, exhibiting a 14% inhibition rate at a concentration of 10 μM.

p38 MAPK-IN-8 (Compound 8) is an orally active, potent, and selective inhibitor of p38 mitogen-activated protein kinase (p38 MAPK). It holds potential for research in inflammatory responses, autoimmune diseases, and cancer.

p38 MAPK-IN-7 (Compound 2) is an orally active and potent inhibitor of p38 MAP kinase, with an IC50 of 170 nM. It holds potential in the study of inflammatory diseases, including rheumatoid arthritis and septic shock.

p38 MAPK-IN-10 (Compound 4) is an orally active and potent inhibitor of p38 MAP kinase, with an IC50 of 570 nM. It shows promise for research into chronic inflammatory diseases, including rheumatoid arthritis and Crohn's disease.

(S)-p38 MAPK inhibitor III is a methylsulfanylimidazole that inhibits p38 MAP kinase (IC50 = 0.90 μM in vitro). It is cell-permeable, potently blocking the release of TNF-α and IL-1β from human peripheral blood mononuclear cells (IC50s = 0.37 and 0.044 μM, respectively).

ERK2/p38α MAPK-IN-1 (Compound 1, In silico Hit-2), a selective inhibitor of ERK2 and p38α MAPK, exhibits potent activity with an IC 50 of 82 μM against ERK2. It uniquely binds to the allosteric sites of both ERK2 and p38α MAPK. This compound is utilized for type 2 diabetes research [1].

SB 202190 (FHPI) is a p38 MAPK inhibitor that inhibits p38α and p38β2 (IC50=50/100 nM) selectively and cell-permeably. SB 202190 has antitumor activity and also induces the differentiation of human embryonic stem cells into cardiomyocytes.

Doramapimod (BIRB 796) is a highly potent inhibitor of p38 MAPK (Kd: 0.1 nM), but weakly inhibits c-RAF, Fyn, Lck, ERK-1, SYK, IKK2, and ZAP-70.

Adezmapimod (SB 203580) is a selective, ATP-competitive p38 MAPK inhibitor (IC50=0.3-0.5 μM) that activates autophagy and mitochondrial autophagy, with more than 100-fold higher selectivity over PKB, LCK, and GSK-3β.

Semaglutide is a long-acting, selective, competitive GLP-1R agonist and a long-acting analog of human glucagon-like peptide-1, exhibiting potent hypoglycemic, weight-loss, cardioprotective, and neuroprotective effects. Upon activation of the GLP-1R, semaglutide promotes insulin secretion, inhibits gastric emptying and appetite, while also enhancing autophagy and suppressing oxidative stress and apoptosis. Semaglutide also plays a role in regulating mitochondrial function and lipid metabolism. Semaglutide is being investigated for use in type 2 diabetes, obesity, Parkinson’s disease, metabolic and fatty liver diseases (MASLD), and other neurodegenerative and liver diseases, as well as in cancer research.

Semaglutide Acetate is a GLP-1R agonist (EC50=6.2 pM) with long-acting, selective, competitive, and oral efficacy. Semaglutide acetate can be used in the study of type 2 diabetes.

Semaglutide sodium is a glucagon-like peptide-1 (GLP-1) receptor agonist that exerts its blood glucose-lowering effect by mimicking GLP-1. It promotes pancreatic beta-cell function and insulin secretion while inhibiting glucagon release, thereby reducing hepatic glycogenolysis and gluconeogenesis. In addition, Semaglutide sodium slows gastric emptying and reduces appetite, thereby decreasing energy intake and promoting weight loss.

PAF (C16) is a potent MAPK and MEK/ERK activator that induces increased vascular permeability. PAF (C16) (PAF (C16)) is a platelet-activating factor, a phospholipid-derived mediator and a ligand for PAF G protein-coupled receptor (PAFR). PAF (C16) has shown anti-apoptotic and anti-inflammatory activity in vitro, inhibiting Caspase-dependent apoptosis by interacting with its receptor (PAF-R) to perform cell signaling.

p-Cresyl Sulfate is the major uremic toxin present in the blood of patients with chronic kidney disease and is derived from the metabolites of tyrosine and phenylalanine in the liver.

Cytochalasin D is an actin inhibitor, the removal of actin stress fibers is crucial for the chondrogenic differentiation. It may be an inhibitor of some fertilization processes such as sperm penetration or sperm head decondensation. Cytochalasin D inhibit

1. Dehydrocorydaline (13-Methylpalmatine) exerts anti-metastatic potential via suppression of MMPs and Bcl-2 signaling in NSC-LC cells. 2. Dehydrocorydaline stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. 3. Dehydrocorydaline shows antiplatelet effects, it inhibits thrombin-induced platelet aggregation in a low dose ( IC50= 34.914 ug/mL). 4. Dehydrocorydaline has anti-inflammatory and antinociceptive effects. 5. Dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.