peritonitis

Dicloxacillin Sodium hydrate is a narrow-spectrum β-Lactam antibiotic of the penicillin class, used to treat infections caused by susceptible Gram-positive bacteria.

BMS-813160 is the first dual CCR2/CCR5 antagonist to enter Clinical development for cardiovascular.

GS-441524 treatment of cats with naturally occurring feline infectious peritonitis.

Cloxacillin sodium monohydrate (Cloxacillin Sodium) is the sodium salt of cloxaclliin, a semisynthetic beta-lactamase resistant penicillin antibiotic with antibacterial activity.

AA 2379 is an orally available antirheumatic agent with anti-inflammatory and antipyretic activity that dose-dependently inhibits complement-mediated yeast glycan-induced paw edema in rats and yeast glycan-activated serum-induced peritonitis in mice.

Sodium thioglycolate is a biochemical reagent with disulfide-reducing properties, used as a biomaterial or organic compound in life science research, and is commonly employed to induce peritonitis models.

NDM-1 inhibitor-7 (Compound A8) is an NDM-1 inhibitor with an IC50 of 10.284 μM. It restores the ability of meropenem (MEM) to penetrate the cell wall of Gram-negative bacteria and effectively reinstates MEM's antibacterial activity against NDM-1 positive Escherichia coli. Moreover, NDM-1 inhibitor-7 demonstrates significant efficacy in both Galleria mellonella and murine peritonitis infection models.

NLRP3-IN-75 is an orally effective inhibitor of NLRP3, capable of suppressing IL-1β secretion with an IC50 of 23 nM. It selectively inhibits NLRP3 activation by disrupting inflammasome assembly without affecting the assembly of NLRC4 or AIM2 inflammasomes. NLRP3-IN-75 demonstrates excellent anti-inflammatory effects in models of acute peritonitis, diabetic nephropathy, and inflammatory bowel disease (IBD).

AS-605240 (potassium) is an orally active PI3Kγ inhibitor with an IC50 of 8 nM and a Ki of 7.8 nM. It inhibits MCP-1 and CSF1-induced PKB phosphorylation with IC50 values of 0.181 µM and 0.550 µM, respectively. In mouse models of peritonitis induced by RANTES (CCL5) and thioglycolate, AS-605240 (potassium) reduces neutrophil recruitment, showing EC50 values of 9.1 mg/kg and 10 mg/kg. Additionally, AS-605240 (potassium) ameliorates arthritis induced by αCII-IA in mice.

NLRP3-IN-79 (Compound B6) is a selective inhibitor of the NLRP3 inflammasome with an IC50 value of 10.69 nM. It blocks the assembly of the NLRP3 inflammasome by disrupting the interaction between NEK7 and NLRP3. NLRP3-IN-79 shows potential for research in NLRP3-driven inflammatory diseases such as systemic inflammation, peritonitis, and colitis.

HDAC6-IN-54 (Compound 9m) is a highly selective inhibitor of HDAC6 (histone deacetylase 6), with an IC50 value of 0.021 μM. It prevents the activation of the NLRP3 inflammasome, providing relief from symptoms associated with NLRP3 inflammasome-related diseases such as acute peritonitis, inflammatory bowel disease, and psoriasis.

ZY39 is a selective casein protease P (ClpP) agonist that inhibits the growth of multidrug-resistant strains by selectively activating Staphylococcus aureus ClpP (SaClpP). ZY39 also promotes the enzymatic hydrolysis of human ClpP (HsClpP) in vitro. ZY39 inhibits the growth of multidrug-resistant strains in a mouse peritonitis model of Staphylococcus aureus infection. ZY39 can be used in research related to Staphylococcus aureus infections.

MAO-A/B-IN-4 is an orally active inhibitor of MAO-A/B with IC50 values of 51.3 μM and 47.0 μM, respectively. It demonstrates potent activity against S. aureus, MSSA, MRSA, LRSA, and LREFa. In a mouse model of LRSA peritonitis infection, MAO-A/B-IN-4 shows significant antibacterial efficacy. It is applicable for research into bacterial infections.

NPSR1 antagonist-1 is a potent and peripherally restricted antagonist of the neuropeptide S receptor 1 (NPSR1). It can inhibit the expression of IL-6, PTGS2, IL-20, and CXCL8, and it also reduces TNF-α cytokine levels. NPSR1 antagonist-1 is useful in inflammation-related research, such as peritonitis studies.

NLRP3-IN-84 (Compound 32) is an inhibitor of the NLRP3 inflammasome. It interferes with the oligomerization of NLRP3 by inhibiting the activity of NLRP3ATPase (IC50= 158.4 nM). NLRP3-IN-84 also inhibits Caspase-1 (IC50= 27.7 nM), the release of IL-1β in PBMC (IC50= 19.5 nM) and mPBMC (IC50= 24.2 nM), and ASC speck formation (IC50= 131 nM). It shows no inhibitory activity against the NLRC4 and AIM2 inflammasomes. NLRP3-IN-84 exhibits significant in vivo anti-inflammatory effects in a mouse acute peritonitis model, making it useful for studying NLRP3-related inflammatory diseases.

CAI0019 is an orally active α-carbonic anhydrase inhibitor based on the Acetazolamide framework. This compound has narrow-spectrum activity against enterococci, with a MIC50 of 0.094 μM and a MIC90 of 0.39 μM. In a mouse model of septic peritonitis, CAI0019 selectively inhibits enterococci without affecting most gut commensal bacteria.

Benzo-17R-RvD2 is a benzo analog of RvD2 that enhances phagocytosis in human macrophages, limits neutrophil infiltration, lowers TNF-α levels, and increases the activity of IL-1 receptor antagonists during peritonitis. It promotes human leukocyte E. coli killing and reduces neutrophil aggregation area without affecting anti-Candida activity. Benzo-17R-RvD2 activates the human RvD2 receptor with an EC50 of approximately 1.5 nM. This compound is applicable in the research of inflammation-related diseases, including cardiovascular diseases, cancer, neuroinflammation, pain, and muscle regeneration.

sEH/FLAP-IN-2 is a selective dual inhibitor of sEH (IC50 = 12.6 nM) and FLAP. It significantly reduces lipids derived from 5-LOX/FLAP and sEH, thereby promoting the redistribution of these lipids. sEH/FLAP-IN-2 is applicable in peritonitis research.

A-987306 is a potent and orally bioavailable histamine H4 antagonist with Kis of 3.4 nM and 5.8 nM for rat H4 and human H4, respectively. A-987306 exhibits anti-inflammatory activity in a mouse peritonitis model [1].

Resolvin E2 (RvE2) is a member of the specialized pro-resolving mediator (SPM) family of bioactive lipids.1It is produced from eicosapentaenoic acidviaan 18-HEPE intermediate, which is formed by aspirin-acetylated COX-2-mediated oxidation of EPA, by 5-lipoxygenase (5-LO) in human polymorphonuclear (PMN) neutrophils.2,3RvE2 (20 ng/animal) inhibits increases in inflammatory exudate neutrophil infiltration in a mouse model of peritonitis induced by zymosan A .3Hepatic RvE2 levels are increased in mice fed normal chow, as well as in a mouse model of high-fat diet-induced non-alcoholic fatty liver disease (NAFLD), by dietary supplementation with EPA.4Plasma levels of RvE2 are increased by dietary supplementation with fish oil containing ω-3 polyunsaturated fatty acids (PUFAs) in patients with peripheral artery disease or chronic kidney disease.1,5,6 1.Chiang, N., and Serhan, C.N.Specialized pro-resolving mediator network: An update on production and actionsEssays Biochem.64(3)443-462(2020) 2.Tjonahen, E., Oh, S.F., Siegelman, J., et al.Resolvin E2: Identification and anti-inflammatory actions: Pivotal role of human 5-lipoxygenase in resolvin E series biosynthesisChemistry & Biology131193-1202(2006) 3.Sungwhan, F.O., Pillai, P.S., Recchiuti, A., et al.Pro-resolving actions and stereoselective biosynthesis of 18S E-series resolvins in human leukocytes and murine inflammationJ. Clin. Invest.121(2)569-581(2011) 4.Echeverría, F., Valenzuela, R., Espinosa, A., et al.Reduction of high-fat diet-induced liver proinflammatory state by eicosapentaenoic acid plus hydroxytyrosol supplementation: Involvement of resolvins RvE1/2 and RvD1/2J. Nutr. Biochem.6335-43(2019) 5.Ramirez, J.L., Gasper, W.J., Khetani, S.A., et al.Fish oil increases specialized pro-resolving lipid mediators in PAD (the OMEGA-PAD II trial)J. Surg. Res.238164-174(2019) 6.Barden, A.E., Shinde, S., Burke, V., et al.The effect of n-3 fatty acids and coenzyme Q10 supplementation on neutrophil leukotrienes, mediators of inflammation resolution and myeloperoxidase in chronic kidney diseaseProstaglandins Other Lipid Mediat.1361-8(2018)

Resolvins are a family of potent lipid mediators derived from both eicosapentaenoic acid and docosahexaenoic acid.[1] In addition to being anti-inflammatory, resolvins promote the resolution of the inflammatory response back to a non-inflamed state.[2] Resolvin D1 is produced physiologically from the sequential oxygenation of DHA by 15- and 5-lipoxygenase.[1] 17(R)-RvD1 is an aspirin-triggered epimer of RvD1 that reduces human polymorphonuclear leukocyte (PMN) transendothelial migration, the earliest event in acute inflammation, with equipotency to RvD1 (EC50 = ~30 nM).[3] 17(R)-RvD1 exhibits a dose-dependent reduction in leukocyte infiltration in a mouse model of peritonitis with maximal inhibition of ~35% at a 100 ng dose.[3] In contrast to RvD1, the aspirin-triggered form resists rapid inactivation by eicosanoid oxidoreductases. Analytical and biological comparisons of synthetic 17(R)-RvD1 with endogenously derived 17(R)-RvD1 have confirmed its identity as matching the natural product.[4]

17(R)-Protectin D1 is an aspirin-triggered epimer of the specialized pro-resolving mediator protectin D1 .1It decreases leukotriene B4-induced transendothelial migration of human polymorphonuclear (PMN) neutrophils when used at concentrations ranging from 0.1 to 10 nM. 17(R)-Protectin D1 (0.01-10 ng) reduces the recruitment of neutrophils in a mouse model of TNF-α-induced peritonitis. 1.Serhan, C.N., Fredman, G., Yang, R., et al.Novel proresolving aspirin-triggered DHA pathwayChem. Biol.18(18)976-987(2011)

Resolvin conjugate in tissue regeneration 1 (RCTR1) is a specialized pro-resolving mediator (SPM) biosynthesized from docosahexaenoic acid by isolated human macrophages and apoptotic polymorphonuclear (PMN) neutrophils.1It has been found in human spleen and bone marrow.2RCTR1 is produced via lipoxygenase-mediated oxidation of DHA to 7(S)-8-epoxy-17(S)-HDHA, which is conjugated to glutathione.1,2,3RCTR1 (10 nM) increases phagocytosis ofE. colior apoptotic neutrophils in isolated human monocyte-derived macrophages.2It decreases chemotaxis induced by leukotriene B4in isolated human neutrophils when used at a concentration of 10 nM. RCTR1 (1 and 10 nM) accelerates tissue regeneration in planaria. Intraperitoneal administration of RCTR1 (100 ng/animal) shortens the inflammatory resolution period and decreases inflammatory exudate neutrophil infiltration in a mouse model ofE. coli-induced peritonitis. 1.Dalli, J., Ramon, S., Norris, P.C., et al.Novel proresolving and tissue-regenerative resolvin and protectin sulfido-conjugated pathwaysFASEB J.29(5)2120-2136(2015) 2.de la Rosa, X., Norris, P.C., Chiang, N., et al.Identification and complete stereochemical assignments of the new resolvin conjugates in tissue regeneration in human tissues that stimulate proresolving phagocyte functions and tissue regenerationAm. J. Pathol.188(4)950-966(2018) 3.Rodriguez, A.R., and Spur, B.W.First total synthesis of pro-resolving and tissue-regenerative resolvin sulfido-conjugatesTetrahedron Lett.58(16)1662-1668(2017)

Protectin conjugates in tissue regeneration 1 (PCTR1) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid . DHA is oxidized to 16S,17S-epoxy-protectin, which is then converted to PCTR1 by glutathione S-transferase. PCTR1 levels increase during resolution of acute microbial-induced peritonitis in mice. PCTR1 (30 ng, i.p.) administration 12 hours post-infection increases macrophage numbers and activity and shortens the resolution phase of inflammation by 57%. It also reduces the levels of PGE2 , PGD2 , and TXB2 in peritoneal exudates.