mi-2

MI-2 (Menin-MLL Inhibitor) is an effective menin-MLL interaction inhibitor (IC50: 446 ± 28 nM).

MI-2 (MALT1 inhibitor) is an irreversible MALT1 inhibitor.

Menin-MLL inhibitor MI-2 (MI2) is a potent menin-MLL interaction inhibitor with IC50 of 446 nM.

Menin-MLL inhibitor MI-2 dihydrochloride is a competitive and selective inhibitor of the Menin-MLL interaction, with an IC50 value of 446 nM and a Ki value of 158 nM. It reduces the expression of target genes such as HOXA9 and MEIS1, inhibits the proliferation of leukemic cells, and induces apoptosis and differentiation. Menin-MLL inhibitor MI-2 dihydrochloride shows potential for research in MLL-rearranged acute leukemias, such as acute myeloid leukemia and acute lymphoblastic leukemia.

MI-2-2 is an inhibitor of bivalent protein-protein interaction between menin and MLL with an IC50 of 46 nM. MI-2-2 binds to menin with Kd of 22 nM.

MI-219 is a human double minute 2 (HDM2) inhibitor.

OSMI-2 is a cell-permeable inhibitor of O-linked N-acetylglucosamine transferase (OGT).

MI-217 is an effective SIRT3 inhibitor that induces apoptosis in MDA-MB-231 cells. It is applicable for breast cancer research.

p18SMI-21 is a novel INK4C inhibitor. It also specifically blocking the bioactivity of p18 protein.

p18SMI-22 is an INK4C inhibitor.

MI-223 is an inhibitor of Mcl-1-stimulated homologous recombination (HR) DNA repair, which leads to sensitization of cancer cells to hydroxyurea- or olaparib-induced DNA replication stress.

MI-192 is a selective HDAC2 and HDAC3 inhibitor with IC50 values of 30 nM and 16 nM, respectively. It exhibits greater selectivity for HDAC2/3 over other HDAC isomers and induces apoptosis in myeloid leukemic cells, indicating potential therapeutic use in leukemia and as an anti-stroke agent [1] [2].

MI-773 (SAR405838 (MI 773)) is an orally available MDM2 antagonist with Ki of 0.88 nM. Phase 1.

L-2-Hydroxyglutaric acid disodium ((S)-2-Hydroxyglutaric acid disodium) is an epigenetic modifier and putative oncometabolite in renal cancer. L-2-Hydroxyglutaric acid inhibits mitochondrial creatine kinase (Mi-CK) activity(Km and Ki of 2.52 mM and 11.13 mM, respectively).

Geroquinol (geranylhydroquinone) functions as a radioprotective agent.

MI-1063 is a DMD-2 inhibitor that prevents the MDM2-p53 interaction and activates p53's tumor-suppressing abilities. It inhibits the growth of cancer cells RS4-11 and MV4-11, with IC50 values of 179 nM and 93 nM, respectively. MI-1063 serves as a target protein ligand for the synthesis of the PROTAC degrader [MD-265].

ALDH2activator 1 (Compound Z17) is an allosteric activator of aldehyde dehydrogenase 2 (ALDH2). This compound improves cardiac function and reduces myocardial necrosis in a mouse model of ischemia-reperfusion. ALDH2activator 1 holds potential for research in cardiovascular diseases, such as myocardial infarction (MI).

Methylisothiazolinone is a powerful synthetic biocide and preservative.

MI-1851 is a potent peptidomimetic inhibitor. MI-1851could prevent proteolytic processing of the S protein from SARSCoV-2 by endogenous furin in HEK293 cells.

SR-33805 is a calcium channel antagonist potentially for the treatment of atherosclerosis and heart failure. SR-33805 restored the MI-altered cell shortening without affecting the Ca(2+) transient amplitude, suggesting an increase of myofilament Ca(2+) sensitivity in MI myocytes. A SR33805-induced sensitization of myofilament activation was found to be associated with a slight increase in myosin light chain-2 phosphorylation and a more significant decrease on troponin I (TnI) phosphorylation. Decreased TnI phosphorylation was related to inhibition of protein kinase A activity by SR-33805.

Delcasertib (KAI-9803) hydrochloride, a potent and selective δ-protein kinase C (δPKC) inhibitor, shows promise in reducing ischemia and reperfusion injury in animal models of acute myocardial infarction (MI) [1] [2].

ROS-IN-2 (compound 85), a seco-lupane triterpenoid derivative, inhibits reactive oxygen species (ROS) production and shields mitochondria from oxidative damage by curtailing the generation of oxidative stressors. It has applications in myocardial ischemia/reperfusion (MI/R) injury research [1].