md 2

MD2-TLR4-IN-1 is a myeloid differentiation protein 2/toll-like receptor 4 (MD2-TLR4) complex inhibitor.

MD2-IN-1 is a Myeloid differentiation protein 2 (MD2) inhibitor with a KD of 189  μM for the recombinant human MD2 (rhMD2).

Hisphen shows antileukemic activity.

2MD, an orally active vitamin D analog, both stimulates periosteal bone formation and decreases trabecular bone resorption, effectively restoring trabecular and cortical bone mass and strength. Additionally, 2MD regulates genes related to intraocular pressure (IOP) and reduces IOP in non-human primates [1] [2].

1. Atractylenolide-I has an anti-inflammatory effect by inhibiting TNF-α and IL-6 production; ameliorates sepsis syndrome, liver and kidney functions by reduction of pro-inflammatory cytokines and LPS. 2. Atractylenolide-I significantly sensitizes the res

1. Isofraxidin (Phytodolor) protects leukemia cells from radiation-induced apoptosis via ROS mitochondria pathway in a p53-independent manner. 2. Isofraxidin has a protective effect against LPS-induced ALI, and the protective effect of Isofraxidin seems to result from the inhibition of COX-2 protein expression in the lung, which regulates the production of PGE2. 3. Isofraxidin possesses significant analgesic and anti-inflammatory activities that may be mediated through the regulation of pro-inflammatory cytokines, TNF-α and the phosphorylation of p38 and ERK1 2.

MD-222, a pioneering, highly potent PROTAC degrader targeting MDM2, efficiently mediates the rapid degradation of MDM2 protein and activates wild-type p53 within cells, showcasing significant anticancer effects[1][2].

Neoseptin 3 is an agonist of Toll-like receptor 4/myeloid differentiation factor 2 (EC50: 18.5 μM).

L6H21 is an MD-2 inhibitor that can be used to study cognitive impairment and brain damage.

MD-224 is a highly potent and efficacious MDM2 degrader based on the proteolysistargeting chimera (PROTAC) concept,and as a new class of anticancer agent.

NF-κB-IN-8 is a competitive antagonist of LPS for MD-2 binding, and it impedes the expression of inflammatory factors by engaging MD-2. Additionally, it inhibits ALP activity and is usable in inflammation research, including acute lung injury (ALI) [1].

Tat-CIRP, a peptide inhibitor, impedes the protein-protein interaction between myeloid differentiation 2 (MD-2), also known as lymphocyte antigen 96 (LY96), and cold-inducible RNA binding protein (CIRP) by binding to MD-2. This disrupts the MD-2 and CIRP interaction as confirmed in co-immunoprecipitation assays. Notably, in vivo studies reveal that Tat-CIRP, at dosages of 10 and 20 mg/kg, significantly reduces infarct volume in both a mouse model of middle cerebral artery occlusion (MCAO) and a rhesus monkey model of thrombosis-induced stroke. Additionally, it improves motor function, evidenced by decreased time to manipulate and withdraw food with the affected arm in the primate model.

Collismycin A is a bacterial metabolite from *Streptomyces* with antibacterial, antiproliferative, and neuroprotective properties. It exhibits activity against various bacteria (MICs = 6.25-100 μg ml) and fungi (MICs = 12.5-100 μg ml). It inhibits proliferation of A549 lung, HCT116 colon, and HeLa cervical cancer cells (IC50s = 0.3, 0.6, and 0.3 μM, respectively) and NIH373 fibroblasts (IC50 = 56.6 μM) but not MDA-MD-231 breast cancer cells (IC50 > 100 μM). Collismycin A forms a complex with Fe(II) and Fe(III) in a 2:1 ratio, with iron ions inhibiting its antiproliferative effect on HeLa cells, an effect not observed with zinc, manganese, copper, or magnesium ions. Additionally, Collismycin A (1 μM) reduces apoptosis in zebrafish larvae brain regions by 44% in a model of neuronal cell death induced by all-trans retinoic acid.

Procyanidin B1, isolated from commonly eaten fruits, binds to the TLR4 MD-2 complex and has anti-inflammatory activity.

TAT-CIRP, a trans-activating (Tat) cold-inducible RNA-binding protein-derived peptide, functions as an inhibitor of myeloid differentiation protein 2 (MD2). It has demonstrated significant neuroprotective effects against ischemic and hemorrhagic stroke in mouse models [1].