peritonitis

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.

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.

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

1. β-Anhydroicaritin exhibits immunosuppressive effect on the mouse macrophages stimulated by LPS. 2. β-Anhydroicaritin phytosomes can inhibit enhanced bone turnover induced by ovariectomy, improve BMD the biomechanical properties of vertebrae, without any stimulation on uterus. 3. β-Anhydroicaritin possesses significant protective effects on the zymosan-induced peritonitis mice, which might be associated with the regulation of Ca(2+); influx in macrophages and iNOS expression.

Protectin D1 (also known as neuroprotectin D1 when produced in neuronal tissues) is a DHA-derived dihydroxy fatty acid that exhibits potent protective and anti-inflammatory activities. 10(S),17(S)-DiHDHA is a DHA metabolite, also referred to as protectin DX (PDX). It is produced by an apparent double lipoxygenase (LO)-mediated reaction in murine peritonitis exudates, in suspensions of human leukocytes, or by soybean 15-LO incubated with DHA. It differs from protectin D1 with respect to the stereochemistry of the C-10 hydroxyl and the double bond configuration at the 13 and 15 positions. 10(S),17(S)-DiHDHA blocks neutrophil infiltration in murine peritonitis by 20-25% at a dose of 1 ng/mouse. It also inhibits platelet activation by both impairing thromboxane (TX) synthesis and TX receptor activation.

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

GS-441524 was shown to be a safe and effective treatment for feline infectious peritonitis (FIP). The optimum dosage was found to be 4.0 mg kg SC q24h for at least 12 weeks

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.

NP3-562 is a powerful, orally administered tricyclic NLRP3 inhibitor, demonstrating an IC₅₀ of 214 nM. At a dosage of 30 mg kg given orally (p.o.), NP3-562 effectively suppresses IL-1β release in a mouse model of acute peritonitis [1].

Prostaglandin E2 (PGE2) inhibitor 3 is a selective inhibitor targeting microsomal prostaglandin E synthase-1 (mPGES-1; IC50 = 0.2 µM), demonstrating greater selectivity for mPGES-1 over COX-1, COX-2, 5-lipoxygenase (5-LO), and soluble epoxide hydrolase (sEH) in assays at 10 µM. This compound effectively reduces IL-1β-induced PGE2 production in A549 cells and decreases LPS-induced IL-6 and PGE2 in J774A.1 macrophages at concentrations of 10 and 1 µM, respectively. Additionally, it blocks the production of 5-LO-derived products, including leukotriene B4 (LTB4) and 5-H(p)ETE, in response to calcium ionophore A23187 alone or combined with arachidonic acid, with IC50 values of 4.9 and 5.2 µM, respectively. When administered in vivo at doses of 10 mg/kg, PGE2 inhibitor 3 effectively prevents leukocyte infiltration in a mouse model of zymosan-induced peritonitis.

NLRP3-IN-34 (Compound T10) acts as an inhibitor of the NLRP3 inflammasome. It blocks the production of reactive oxygen species (ROS) and impedes the formation of NLRP3 inflammasome-dependent IL-1β (J774A.1, IC50 of 0.48 μM), while also inhibiting pyroptosis (cell suicide). Additionally, NLRP3-IN-34 displays anti-inflammatory activity in a C57BL 6 mouse model for DSS-induced peritonitis.

Maresin conjugates in tissue regeneration 1 (MCTR1) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages at the site of inflammation. DHA is oxidized to maresin 1 , which is then converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase. MCTR1 accelerates tissue regeneration in planaria (1 and 100 nM). Pretreatment with MCTR1 (50 ng/mouse, i.p.) prior to E. coli administration reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR1 reduces the amount of eicosanoids in the exudate.

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].

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)

Maresin conjugates in tissue regeneration 3 (MCTR3) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages. DHA is oxidized to maresin 1 , which is converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase, then to MCTR2 by γ-glutamyl transferase, and to MCTR3 by dipeptidase. MCTR3 accelerates tissue regeneration in planaria (1 and 100 nM) approximately as potently as MCTR2 and more potently than MCTR1. Pretreatment with MCTR3 prior to E. coli administration in mice reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR3 selectively reduces the amount of the eicosanoids PGD2 , PGE2 , PGF2α , and TXB2 in the exudate.

Maresin 2 (3R,14S-diHDHA) is a specialized pro-ablative lipid mediator (SPM) with anti-inflammatory and analgesic activity, promotes mucosal repair, and reduces neutrophil recruitment in yeast polymerase peritonitis.

Resomelagonmethanesulfonate (AP1189 methanesulfonate) is the methanesulfonate salt form of Resomelagon. It is an orally active melanocortin receptor (MR) agonist that induces ERK1 2 phosphorylation and Ca2+ mobilization. In mouse models of peritonitis and arthritis, Resomelagonmethanesulfonate demonstrates anti-inflammatory activity and can be used for research on obesity and chronic inflammation.

Invopressin (Compound 42), a vasopressin V1A receptor partial agonist (EC50: 1.0 nM), is utilized in research related to cirrhosis conditions such as bacterial peritonitis, HRS2, and refractory ascites [1].

Plectasin, a peptide antibiotic derived from saprophytic fungi, can effectively kill Streptococcus pneumoniae in vitro. Additionally, it alleviates experimental peritonitis and pneumonia caused by Streptococcus pneumoniae in mice.

Zharp2-1, a RIPK2 inhibitor, inhibits the transcription of inflammatory cytokines induced by MDP-induced or Listeria monocytogenes infection and alleviates MDP-induced peritonitis symptoms in mice, which can be used for the study of inflammatory bowel disease (IBD).

Maresin conjugates in tissue regeneration 2 (MCTR2) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid in macrophages at the site of inflammation. DHA is oxidized to maresin 1 , which is converted to MCTR1 by glutathione S-transferase Mu 4 or leukotriene C4 synthase then to MCTR2 by γ-glutamyl transferase. MCTR2 accelerates tissue regeneration in planaria (1 and 100 nM). Pretreatment with MCTR2 prior to E. coli administration reduces neutrophil infiltration, shortens the inflammatory resolution period, and increases phagocytosis of E. coli by macrophages. When administered at a dose of 100 ng 12h post E. coli infection in a mouse model of peritonitis, MCTR2 selectively reduced the amount of the eicosanoids PGD2 and PGF2α in the exudate.

17(R)-Resolvin D1 (17(R)-RvD1) is an aspirin-triggered epimer of RvD1 that equivalently inhibits human polymorphonuclear leukocyte migration across the endothelium (EC50= ~30 nM), a precursor to acute inflammation. Unlike RvD1, it resists rapid degradation by eicosanoid oxidoreductases. In a mouse peritonitis model, 17(R)-RvD1 dose-dependently reduces leukocyte infiltration, achieving up to a 35% decrease with a 100 ng dose. Additionally, its methyl ester derivative, designed to enhance its pharmacokinetic and distribution properties as a more lipophilic prodrug, can be converted back into the active acid form by intracellular esterases.

Resolvin E4 (RvE4) is a member of the specialized pro-resolving mediator (SPM) family of bioactive lipids.1It is produced from eicosapentaenoic acid by 15-lipoxygenase (15-LO)via15(S)-HpEPE and 15S-hydroxy, 5S-HpEPE intermediatesin vitroand by isolated human M2 macrophages or polymorphonuclear (PMN) neutrophils under normoxic or hypoxic conditions. RvE4 synthesis is enhanced in M2 macrophage and neutrophil co-cultures, indicating transcellular biosynthesis by a potential 15-LO and 5-LO mechanism. It has been found in mouse inflammatory exudates. RvE4 (10 nM) increases efferocytosis of apoptotic neutrophils or senescent red blood cells (sRBCs) by human M2 macrophages under hypoxic conditionsin vitro. Intraperitoneal administration of RvE4 (100 ng/animal) inhibits increases in inflammatory exudate neutrophil infiltration in a mouse model of hemorrhagic peritonitis induced by zymosan A and thrombin. It also increases inflammatory exudate macrophage infiltration and efferocytosis of apoptotic neutrophils and/or RBCs in the same model. 1.Norris, P.C., Libreros, S., and Serhan, C.N.Resolution metabolomes activated by hypoxic environmentSci. Adv.5(10)eaax4895(2019)