Safinamide mesylate (EMD 1195686 mesylate) , a mesylate salt of Safinamide, can reversibly and specifically inhibit MAO-B (IC50: 98 nM), has 5918-fold selectivity against MAO-A.

3-Aminobenzamide (PARP-IN-1) is an effective inhibitor of PARP (IC50<50 nM in CHO cells) and a mediator of oxidant-induced myocyte dysfunction during reperfusion.

Sodium Hydrogen Sulfide (hydrate) is, like nitric oxide, an important gaseous mediator that has significant effects on the immunological, neurological, cardiovascular and pulmonary systems of mammals. Sodium Hydrogen Sulfide (hydrate) is an H2S donor commonly used in cellular and whole animal experimental systems. For example, it has been used to suggest that H2S promotes neutrophil migration, reduces airway inflammation, and protects neurites, heart, and intestine from chemical or ischemic-reperfusion damage.

NLRP3-IN-2 (5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide), an intermediate capable of synthesizing glibenclamide, exerts an inhibitory effect on the formation of NLRP3 inflammatory vesicles in cardiomyocytes, limiting infarct size after myocardial ischemia/reperfusion in mice and has no effect on metabolism.

Astragaloside IV (AS-IV), an active component isolated from Astragalus membranaceus, suppresses the activation of ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2, (MMP)-9 in MDA-MB-231 breast cancer cells. Astragaloside IV is a bioactive saponin first isolated from the dried plant roots of the genus Astragalus, which is used in traditional Chinese medicine.1 It dose-dependently inhibits human adenovirus type 3 (HAdV-3) in A549 cells (IC50 = 23 μM; LC50 = 865 μM).It inhibits replication of HAdV-3 and decreases HAdV-3-induced apoptosis. It has diverse protective effects for the cardiovascular, immune, digestive, and nervous systems. In particular, it reduces myocardial infarct size in dogs when administered prior to coronary ligation and reduces reperfusion arrhythmias in isolated rat hearts.

MEG hemisulfate (Mercaptoethylguanidine hemisulfate) acts as a highly potent and selective suppressor of inducible NO synthase (iNOS), demonstrating EC50 values of 11.5 μM for iNOS, 110 μM for ecNOS, and 60 μM for bNOS in tissue homogenates. It is notably effective as a peroxynitrite scavenger and blocks peroxynitrite-triggered oxidative mechanisms. Furthermore, this compound offers protective benefits across various experimental inflammation prototypes, such as ischemia/reperfusion injury, hemorrhagic shock, periodontitis, inflammatory bowel disease, and both endotoxic and septic shock.

Montelukast sodium (MK0476) is an orally available leukotriene receptor antagonist which is widely used for the prophylaxis and chronic treatment of asthma and has been linked to rare cases of clinically apparent liver injury.

FK-330 (FR-260330) is a novel orally active inducible nitric oxide synthase inhibitor with potential anticancer and antitumor activity that prevents ischemia and reperfusion injury in rat liver transplantation.

FK-330 dihydrate（FR-260330 dihydrate） is a novel orally active inducible nitric oxide synthase inhibitor with potential anticancer and antitumor activity to prevent ischemia and reperfusion injury in rat liver transplantation.

Raxofelast (IRFI-016) is a hydrophilic, non-systemic, vitamin-like antioxidant that reduces ischemia-reperfusion injury in testis. Raxofelast is a good candidate compound for stopping oxidative stress after acute testicular torsion. Raxofelast has the potential to treat diabetic complications and atherosclerosis.

Tirilazad mesylate (U 74006F) is a non-glucocorticoid, lipid peroxidation inhibitor with antiviral activity and neuroprotective activity.Tirilazad mesylate confines intracellular intramembranous foci, attenuates spinal cord injury induced by trauma, stroke, and ischemia/reperfusion injuries, inhibits toxins in dogs, reduces the effects of Tirilazad mesylate is used in the study of neurological disorders.

Protectin D1 (Neuroprotectin D1) is a neuroprotectin produced by neuronal cells and is a potential cardioprotective agent.Protectin D1 attenuates myocardial ischemia/reperfusion injury and inhibits imiquimod-induced psoriasis-like skin inflammation by modulating the PI3K/AKT signaling pathway.

SSR69071 is a potent, orally active, and selective inhibitor of neutrophil elastase. SSR69071 displays a higher affinity for human elastase (Ki =0.0168 nM) than for rat (Ki =3 nM), mouse (Ki =1.8 nM), and rabbit (Ki = 58 nM) elastases [2]. SSR69071 reduces myocardial infarct size following ischemia-reperfusion injury [1]. SSR69071 also has the potential for the treatment of chronic obstructive pulmonary diseases, asthma, emphysema, cystic fibrosis, and several inflammatory diseases.

LUF6096 (CF-602) is a potent allosteric enhancer of the adenosine A3 receptor, exhibiting the capability to enhance agonist binding allosterically while demonstrating low orthosteric affinity across adenosine receptors. It displays protective effects in myocardial ischemia/reperfusion injury.

Daltroban (SKF 96148) is a specific thromboxane A2 (TXA2) receptor antagonist. Daltroban shows protective effect in reperfusion injury. Daltroban increase intracellular calcium in vascular smooth muscle cells.

Nelonemdaz (Neu2000) is an NMDA receptor antagonist with antioxidant activity and neuroprotective activity used in the study of cerebral infarction reperfusion injury and acute ischemic stroke.

Montelukast (Singular) is an orally available leukotriene receptor antagonist which is widely used for the prophylaxis and chronic treatment of asthma and has been linked to rare cases of clinically apparent liver injury.

1. Ilexsaponin A (Ilexsaponin A1) shows protective effects on ischemia-reperfusion-induced myocardial injury through anti-apoptotic pathway.

Ac2-26 acetate is an active N-terminal peptide of annexin A1(AnxA1). Ac2-26 acetate decreases AnxA1 protein expression and inhibits the activation of NF-κB and MAPK pathways in the injured lung tissue. Ac2-26 acetate attenuates ischemia-reperfusion-induced acute lung injury.

Liriodenine is a potent inhibitor of topoisomerase II (EC 5.99.1.3) both in vivo and in vitro, it has antitumor, antibacterial and antifungal activities, it can suppress ventricular arrhythmias induced by myocardial ischaemia reperfusion, through inhibiti

Tricarbonyldichlororuthenium(II) dimer, a pharmacological CO donor, prevents ischemia/reperfusion (I/R)-induced oxidative damage to the gastric mucosa by enhancing gastric blood flow (GBF) and reducing DNA oxidation and systemic inflammatory response.

Nangibotide, a TREM-1 receptor inhibitor, modulates the innate immune response and has demonstrated the potential to reduce systemic and localized inflammatory reactions in rodent models of myocardial ischemia-reperfusion [1].

Z-LEHD-FMK is a selective and potent caspase-9 inhibitor that protects against reperfusion injury and slows apoptosis.Z-LEHD-FMK exhibits antitumor and neuroprotective activity, increases the yield of in vitro-produced preimplantation embryos of Bubalus bubalis and alters the cellular stress response.

Echinatin exerts a protective effect against ischemia/reperfusion (I/R)-induced myocardial injury on hearts, this effect may be attributed to the antioxidant and anti-inflammatory activities of this compound. Echinatin can inhibit DNP-ATPase activity whil

(±)14(15)-EET is a metabolite of arachidonic acid that is formed via epoxidation of arachidonic acid by cytochrome P450.[1],[2] It prevents increases in leukotriene B4, ICAM-1, and chemokine (C-C motif) ligand 1 (CCL2) induced by oxidized LDL in primary rat pulmonary artery endothelial cells (RPAECs) when used at a concentration of 1 μM.[3] (±)14(15)-EET induces dilation of preconstricted isolated canine coronary arterioles (EC50 = 0.2 pM).[4] It reduces myocardial infarct size as a percentage of the area at risk in a canine model of ischemia-reperfusion injury induced by left anterior descending coronary artery (LAD) occlusion when administered at a dose of 0.128 mg/kg prior to occlusion or reperfusion.[5] Reference：[1]. Chacos, N., Falck, J.R., Wixtrom, C., et al. Novel epoxides formed during the liver cytochrome P-450 oxidation of arachidonic acid. Biochem. Biophys. Res. Commun. 104(3), 916-922 (1982).[2]. Oliw, E.H., Guengerich, F.P., and Oates, J.A. Oxygenation of arachidonic acid by hepatic monooxygenases. Isolation and metabolism of four epoxide intermediates. J. Biol. Chem. 257(7), 3771-3781 (1982).[3]. Jiang, J.-X., Zhang, S.-J., Xiong, Y.-K., et al. EETs attenuate ox-LDL-induced LTB4 production and activity by inhibiting p38 MAPK phosphorylation and 5-LO/BLT1 receptor expression in rat pulmonary arterial endothelial cells. PLoS One 10(6), e0128278 (2015).[4]. Oltman, C.L., Weintraub, N.L., VanRollins, M., et al. Epoxyeicosatrienoic acids and dihydroxyeicosatrienoic acids are potent vasodilators in the canine coronary microcirculation. Circ. Res. 83(9), 932-939 (1998).[5]. Nithipatikom, K., Moore, J.M., Isbell, M.A., et al. Epoxyeicosatrienoic acids in cardioprotection: Ischemic versus reperfusion injury. Am. J. Physiol. Heart Circ. Physiol. 291(2), H537-H542 (2006).

Baohuoside aglycone possesses cardioprotective effect in prevention of ischemia/ reperfusion injury and reduce the myocardial infraction, the mechnism is due to the reduction of the injury of free radicals. Baohuoside VII in vivo exhibits significant anti

NS309 is a nonselective activator of small- and intermediate-conductance Ca2+-activated K+ (SK/KCa2 and IK/KCa3.1) channels (EC50s range from 0.12-1.2 µM for SK channels and 10-90 nM for IK channels). It can also activate voltage-gated Kv11.1 channels (hE

Torapsel (42-89-glycoprotein; WAY164339), a fusion protein comprising immunoglobulin, is employed in the investigation of ischemia-reperfusion injury prophylaxis.

Ru360, an oxygen-bridged dinuclear ruthenium amine complex, is a selective mitochondrial calcium uptake inhibitor. Ru360 potently inhibits Ca2+ uptake into mitochondria with an IC50 of 0.184 nM. Ru360 binds to mitochondria with high affinity (Kd of 0.34 nM). Ru360 has antiarrhythmic and cardioprotective effects[1][2]. Ru360 permeates slowly into the cell, and specifically inhibits mitochondrial calcium uptake in intact cardiomyocytes and in isolated heart. 1 μm Ru360 is taken up by myocardial cells and accumulated in the cytosol in a biphasic manner[1]. During pelleting hypoxia, Ru360 (10 µM) significantly improves cell viability in wild type cardiomyocytes[3]. Ru360 (15-50 nmol/kg) treatment abolishes the incidence of arrhythmias and haemodynamic dysfunction elicited by reperfusion in a whole rat model. Ru360 administration partially inhibits calcium uptake, preventing mitochondria from depolarization by the opening of the mitochondrial permeability transition pore (mPTP)[1]. [1]. G de J García-Rivas, et al. Ru360, a Specific Mitochondrial Calcium Uptake Inhibitor, Improves Cardiac Post-Ischaemic Functional Recovery in Rats in Vivo. Br J Pharmacol. 2006 Dec;149(7):829-37. [2]. M A Matlib, et al. Oxygen-bridged Dinuclear Ruthenium Amine Complex Specifically Inhibits Ca2+ Uptake Into Mitochondria in Vitro and in Situ in Single Cardiac Myocytes. J Biol Chem. 1998 Apr 24;273(17):10223-31. [3]. Lukas J Motloch, et al. UCP2 Modulates Cardioprotective Effects of Ru360 in Isolated Cardiomyocytes During Ischemia. Pharmaceuticals (Basel). 2015 Aug 4;8(3):474-82.

Z-LEHD-FMK TFA is a specific and irreversible inhibitor of caspase-9, offering protection against detrimental reperfusion injury and moderating apoptosis. Additionally, Z-LEHD-FMK TFA demonstrates its neuroprotective potential in a rat model of spinal cord trauma.

Nangibotide TFA, a TREM-1 receptor inhibitor, modulates the innate immune response and attenuates both systemic and localized inflammatory reactions in rodent models of myocardial ischemia-reperfusion [1].

Phoenixin-14 TFA (PNX-14) is a blood-brain barrier (BBB)-penetrable neuropeptide with anxiolytic, cardioprotective, and neuroprotective properties. It modulates pituitary gonadotrophin release by enhancing gonadotropin-releasing hormone (GnRH) receptor mRNA expression and promotes insulin secretion. Additionally, PNX-14 TFA offers protection against ischemia/reperfusion (IR) injury in mice and combats oxidative stress by diminishing reactive oxygen species (ROS) and elevating glutathione (GSH) levels [1] [2] [3].

TRPC1/6 and Piezo2 inhibitor. Exhibits same effect as L-enantiomer, GsMTx4 (Cat. No. 4912) on TRPC channels. Inhibits mechanosensitive currents by ~70%. Protects against myocardial infarction in mouse ischemia/reperfusion model. Resistant to proteolytic digestion.

Ac2-26 TFA is an active n-terminal peptide in annexin A1 (AnxA1), which can alleviate acute lung injury caused by ischemia-reperfusion.

Anti-MI/R injury agent 1 (compound 18), derived from Panaxatriol, represents an orally administered, potent agent against myocardial ischemia/reperfusion (MI/R) injury. It improves cell viability in cardiomyocytes subjected to oxygen-glucose deprivation and reperfusion (OGD/R)-induced injury. Furthermore, this compound significantly reduces myocardial infarction size, diminishes levels of circulating cardiac troponin I (cTnI), and mitigates cardiac tissue damage in rat models [1].

Eleutheroside has protective effect to myocardial ischemic-reperfusion injury(IRI) in isolated rats.

C3a Receptor Agonist (C3a receptor agonist 1) binds the G protein-coupled C3a receptors (C3aRs) in the immune system complement pathway. Activation of C3aR prevents neutrophils from being mobilized in a model of intestinal ischemia-reperfusion injury. C3aRs are expressed on neural progenitor cells and immature neurons in adult mice. C3a stimulates differentiation of neural progenitor cells in vitro.

CDDO-3P-Im is an orally active inhibitor of necroptosis with chemopreventive effects. CDDO-3P-Im can be used in studies about ischemia/reperfusion.

Tirilazad, a nonglucocorticoid 21-aminosteroid, serves to inhibit lipid peroxidation. It mitigates the effects of trauma-induced brain or spinal cord injury, as well as damage resulting from stroke, ischemia, and reperfusion injury. Additionally, Tirilazad exhibits antiviral properties against nCoV and offers neuroprotection in cases of ischemic stroke. It is also utilized in subarachnoid hemorrhage research [1] [2] [3].

FR 167653 sulfate, an orally active and selective inhibitor of p38 MAPK, is effective in treating inflammation, trauma, and ischemia-reperfusion injury in vivo. It acts as a potent suppressor of TNF-α and IL-1β production through specific inhibition of p38 MAPK activity.

Pinoresinol ((+)-Pinoresinol) has antiinflammatory, hepatoprotective, and fungicidal activities, it can protect pial microcirculation from I-reperfusion injury, to increase nitric oxide release and to reduce oxidative stress preserving pial blood flow distribution; it may exert pharmacologically interesting effects via modulation of the insulin-like signalling pathway in C.elegans. Pinoresinol causes an upregulation of the CDK inhibitor p21(WAF1/Cip1) both at mRNA and protein levels, inhibits NF-kappaB and activating protein 1 (AP-1).

Mitochondrial fusion promoter M1, a modulator of mitochondrial dynamics, enhances mitochondrial function and cellular respiration, and has shown efficacy in reducing brain and cardiac damage in rats suffering from cardiac ischemia/reperfusion injury.

Phoenixin-14 (PNX-14), an active endogenous isoform, induces an anxiolytic effect by activating the AHA GnRH system in mice and protects against ischemia/reperfusion-induced cytotoxicity in microglia [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].

INF200 (compound 5), a sulfonylurea-based inhibitor of NLRP3 and associated pyroptosis, exhibits cardiometabolic benefits in a rat model of high-fat diet (HFD)-induced metaflammation and demonstrates anti-inflammatory effects by reducing IL-1β release in human macrophages at a concentration of 10 μM. Additionally, it enhances glucose and lipid profiles, diminishes systemic inflammation and cardiac dysfunction biomarkers, notably BNP, and ameliorates myocardial damage linked to ischemia/reperfusion injury (IRI) as assessed by hemodynamic parameters [1].

NFPS exerts neuroprotection via glyR alpha1 subunit in the rat model of transient focal cerebral ischaemia and reperfusion. NFPS is a selective and non-competitive glycine transporter-1 (GlyT1) inhibitor (IC50s: 2.8 nM and 9.8 nM for hGlyT1 and rGlyT1, respectively).

Nitric Oxide Synthase (599-613) Blocking Peptide, Bovine Endothelial Cell (Ac-Pro-Tyr-Asn-Ser-Ser-Pro-Arg-Pro-Glu-Gln-His-Lys-Ser-Tyr-Lys-Cys) is a peptide that inhibits the function of NOSs as a result it blocks the production of NO. Because of the invol

PD-166793 is an orally active, potent and selective MMP inhibitor with inhibitory effects on MMP-2, MMP-3 and MMP-13.PD-166793 ameliorates myocardial ischemia and reperfusion injury in a rat model of heart failure.PD-166793 is an orally active, potent and selective MMP inhibitor with inhibitory effects on MMP-2, MMP-3, and MMP-13.

VULM 1457 is a potent ACAT inhibitor. VULM 1457 has remarkable hypolipidaemic activity and improves the overall myocardial ischaemia-reperfusion injury outcomes. VULM1457 significantly reduces production and secretion of adrenomedullin (AM) and down-regulates AM receptors on human hepatoblastic cells.

GGsTop is a non-toxic and irreversible inhibitor of γ glutamyl transpeptidase (GGT) (Ki: 170 μM for Human GGT). GGsTop protects hepatic ischemia-reperfusion injury in the rat model. GGsTop shows Kons of 150±10 and 51±3 /(M·s) against E.coli GGT and human GGT, respectively.

Nicorandil (SG-75)(Ikorel) acts by relaxing the smooth muscle of the blood vessels, especially those of the venous system. It undertakes this through two methods. Firstly, by activating potassium channels, and secondly by donating nitric oxide to activate the enzyme guanylate cyclase. Guanylate cyclase causes activation of cGMP leading to both arterial and venous vasodilatation by de-phosphorylation of the myosin light chain.