ep1

ONO-8713 is a selective prostaglandin E receptor subtype EP1 antagonist used to study diseases of the biblical system and metabolism-related diseases.

EP1-antagonist-1 (EP1 antagonist 1) is an EP1 antagonist (pKi: 7.54; pIC50: 8.5).

EP1013 is a broad-spectrum selective inhibitor of Caspase used in the study of type 1 diabetes.

Peptide containing the 'TGL' motif that corresponds to the C-terminus of GluR1 subunit

EP12, a c-Myc inhibitor and G4 stabilizer, induces apoptosis and DNA damage in multiple myeloma cells while obstructing P65 P50 nuclear translocation by disrupting the NF-κB signaling pathway, effectively inhibiting multiple myeloma growth [1].

ZA3-Ep10, a zwitterionic lipid, is utilized in the formulation of lipid nanoparticles for RNA delivery in vivo and non-viral CRISPR Cas gene editing applications.

TAT-NEP1-40 TFA, a blood-brain barrier-permeable peptide, safeguards PC12 cells against oxygen and glucose deprivation (OGD) and fosters neurite outgrowth. Additionally, it enhances neurological outcomes post-ischemia by curtailing apoptosis in ischemic cerebral tissues. This compound has utility in investigating central nervous system (CNS) injuries, encompassing axonal regeneration and functional recuperation following a stroke [1].

TAT-NEP1-40 acetate, a potential therapeutic for axonal regeneration and functional recovery post-stroke, safeguards PC12 cells from oxygen and glucose deprivation (OGD) and encourages neurite outgrowth. This compound also affords cerebral protection against ischemia reperfusion injury by hindering neuronal apoptosis and can be effectively administered into rat brains [1] [2].

Analog of Pep1-TGL

CEP1347-VHL-02 is a PROTAC that selectively targets MLK3. This compound is composed of the target protein ligand CEP-1347, the E3 ubiquitin ligase ligand (S,R,S)-AHPC-Me, and the PROTAC linker Amino-PEG3-CH2COOH. The participating component responsible for controlling the target protein ligand activity is CEP-1347-acid, whereas the conjugate of the E3 ubiquitin ligase ligand and linker is identified as (S,R,S)-AHPC-Me-CO-CH2-PEG3-NH2.

Pep19-2.5, a synthetic antitoxin peptide, inhibits the intracellular signaling cascade triggered by endotoxins by blocking the activity of lipopeptides (LP) and lipopolysaccharides (LPS) mediated through both transmembrane and cytosolic pattern recognition receptors (PRRs). This action disrupts the signaling pathways that normally result in inflammation and cell pyroptosis [1].

TAT-NEP1-40, a blood-brain barrier (BBB) permeable peptide, confers protection to PC12 cells against oxygen and glucose deprivation (OGD) while promoting neurite outgrowth. Furthermore, it enhances neurologic outcomes post-ischemia by mitigating apoptosis in affected cerebral regions. This compound holds potential for central nervous system (CNS) injury research, including studies on axonal regeneration and post-stroke functional recovery [1].

PEP1 is a biologically active peptide that interacts with POPC supported lipid bilayers (SLBs), binding at low concentrations, while higher concentrations induce POPC SLB lysis.

Pep1-DNP conjugate 9 is a functionalized peptide composed of a DNP-hapten and an FGFR1-binding peptide. It exhibits good affinity for FGFR1, with a dissociation constant (KD) of 5.01 μM. This compound effectively recruits anti-DNP antibodies to the surface of FGFR1-positive cells, inhibits FGF2-induced proliferation of rat skeletal myoblasts, and induces apoptosis. In mouse models, Pep1-DNP conjugate 9 demonstrates antitumor activity.

Prostaglandin E2 (PGE2) is a naturally occurring hormone involved in various physiological processes, such as smooth muscle contraction and relaxation, vasodilation and constriction, blood pressure regulation, and inflammatory regulation.

Omidenepag isopropyl (DE-117) is a selective prostaglandin EP2 receptor agonist and a novel topical ocular blood pressure lowering compound.Omidenepag isopropyl has a weak affinity for EP1, EP2, and FP receptors.Omidenepag isopropyl is used in studies of glaucoma and hypertension. Omidenepag isopropyl can be used to study glaucoma and hypertension.

Prostaglandin E1 (Alprostadil) is the naturally occurring prostaglandin E1 (PGE1) which displays a variety of pharmacologic actions. Prostaglandin E1 is a potent vasodilator agent that increases peripheral blood flow, inhibits platelet aggregation, and induces bronchodilation. Used in the treatment of erectile dysfunction, this agent produces corporal smooth muscle relaxation by binding to PGE receptors, resulting in the activation of adenylate cyclase and the subsequent accumulation of 3'5'-cAMP.

PF-04418948 is a potent EP2 receptor antagonist (IC50 = 16 nM for human EP2 receptors). Displays over 2000-fold selectivity for EP2 receptors over EP1, EP3, EP4, DP1 amd CRTH2 receptors; exhibits <30% binding at a diverse panel of GPCRs and ion channels at a concentration of 10 μM. Inhibits PGE2-induced increases in intracellular cAMP; reverses PGE2-invoked relaxation of mouse trachea (IC50 = 2.7 nM).

Treprostinil diethanolamine (UT-15C) is a potent agonist of EP2, DP1, and IP, with values of 3.6, 4.4, and 32.1 nM for EP2, DP1, and IP, respectively, and 212, 826, 2505, and 4680 nM for EP1, EP4, EP3, and FPKi, respectively. Treprostinil diethanolamine contributes to the upregulation of cAMP, maintaining vascular homeostasis and causing vasodilation in human pulmonary arteries.

ONO-8130 is an orally available antagonist of EP1 receptor.

KAG-308 is an effective selective and orally active agonist of the EP4 receptor (Ki: 2.57 nM and EC50: 17 nM for human EP4 receptor), more selective over EP1, EP2, EP3, and IP receptor. KAG-308 suppresses colitis and promotes histological mucosal healing,

AH 6809 is an antagonist of EP and DP receptors, with Ki values of 1217, 1150, 1597, and 1415 nM for the cloned human EP1, EP2, EP3-III, and DP receptors, respectively, and a Ki of 350 nM for the mouse EP2 receptor.

Butaprost is a chemical compound that functions as a selective agonist for the prostaglandin E receptor (EP2). It exhibits an EC50 of 33 nM and a Ki of 2.4 μM when interacting with the murine EP2 receptor. However, Butaprost demonstrates lower activity against murine EP1, EP3, and EP4 receptors. Furthermore, it effectively attenuates fibrosis by inhibiting the TGF-β/Smad2 signaling pathway [1] [2] [3].