septic

S-Methylisothiourea sulfate ((S)-Methylisothiourea sulfate) 是一种选择性 iNOS 抑制剂，在感染性休克的啮齿动物模型中发挥有益作用。

Ginsenoside Rg4 是分离自Panax ginsengC. A. Meyer 叶子中的一种人参三醇型人参皂苷。人参三醇型人参皂苷具有多种生物活性，包括防腐，抗糖尿病，伤口愈合，免疫刺激和抗氧化活性等。

Hexylresorcinol (4-Hexylresorcinol) 是在植物中发现的一种天然产物，具有抗菌、驱虫、防腐和抗肿瘤活性。它是一种可逆、非竞争性的 α-葡萄糖苷酶抑制剂，有抗 DNA 氧化损伤的保护作用。它可诱导鳞癌细胞凋亡。

2,5-Dihydroxybenzaldehyde (Gentisaldehyde) 是一种天然抗微生物剂，可抑制Mycobacterium avium subsp. paratuberculosis 的生长。它还抑制金黄色葡萄球菌菌株，MIC50为 500 mg L。

Diloxanide furoate (Dichlofurazol) 是一种具有口服活性的抗原生动物化合物，可用于研究组织内阿米巴和其他一些原生动物感染。

BD-AcAc 2 (Ketone Ester) 是一种酮单酯，是口服营养酮的来源。小鼠口服 BD-AcAc 2 后可提高血浆 乙酰乙酸和β-羟基丁酸水平、血液钠离子、血糖水平和血肌酐水平。BD-AcAc 2 可以一定程度预防脓毒症小鼠的肌无力。BD-AcAc 2 显示出提高动物机体耐力和运动能力的潜力。BD-AcAc 2 还可用于研究糖尿病或帕金森病。

MEG hemisulfate (Mercaptoethylguanidine hemisulfate) 是一种有效和选择性的诱导型 NO 合酶 (iNOS) 的抑制剂，在组织匀浆中抑制 iNOS，ecNOS 和 bNOS 的 EC50 值分别为 11.5，110 和 60 μM。MEG hemisulfate 也有效的过氧亚硝酸盐清除剂，可抑制过氧亚硝酸盐诱导的氧化过程。MEG hemisulfate 在许多炎症实验模型中具有保护作用，包括缺血 再灌注损伤，牙周炎，失血性休克，炎性肠病以及内毒素和败血性休克。

Ethyl gallate (gallic acid ethyl ester) 是一种非类黄酮酚过氧化氢清除剂。

SIRT5 inhibitor 7 (compound 58) 是底物竞争性和选择性的 SIRT5 抑制剂，IC 50 = 310 nM，显著减轻了脂多糖（LPS）和盲肠结扎 穿孔（CLP）诱导的脓毒性AKI小鼠的肾功能障碍和病理损伤，调节急性肾损伤（AKI）小鼠肾脏中蛋白琥珀酰化和促炎细胞因子的释放。

Cl-amidine hydrochloride 是一种口服有效的PAD抑制剂，可阻断组蛋白3去亚胺化和中性粒细胞胞外陷阱的形成，并提高败血症小鼠的存活率。它可诱导癌细胞凋亡，还可诱导 miR-16 引起细胞周期阻滞。

RNAIII-inhibiting peptide TFA (RNAIII-inhibiting peptide(TFA))(228544-21-6 free base) 抑制肽（TFA）抑制金黄色葡萄球菌，对蜂窝织炎、角膜炎、化脓性关节炎、骨髓炎和乳腺炎等疾病有效。

Terlipressin Acetate 是一种高度选择性的加压素 V1 受体激动剂，对氧和葡萄糖剥夺 再氧合 (OGD R) 诱导的肠上皮细胞损伤 (IEC-6) 具有抗炎和抗氧化作用，可用于肝肾综合征和耐去甲肾上腺素的败血性休克的研究。

TNF-α IL-1β-IN-1 (compound 11a) 作为一种有效的抗炎化合物，可有效降低TNF-α和IL-1β的活性并抑制氧化应激及心肌细胞凋亡。此外，该化合物对于脓毒性心肌损伤显示出显著的治疗效果，并能改善心肌的血流供应。

BPD 是 COX-2 和 TAK1-NF-κB 的抑制剂，显示对 COX-2 的 IC50 为 18.5 μM。在转录水平上，BPD 能抑制 iNOS、TNF-α、IL-6 和 IL-1β 的表达。BPD 展现出抗炎活性，能够抑制角叉菜胶引起的爪水肿，并减少 LPS 诱导的脓毒症导致的死亡率。

(+)-Bicuculline methiodide 是一种可穿过大鼠血脑屏障（BBB）的 γ-氨基丁酸 A 型 （GABAA) 受体阻断剂，可阻断阻断癫痫原，可用于研究癫痫等神经系统疾病。(+)-Bicuculline methiodide 可降低脓毒症大鼠的肝损伤。

Tanogitran, a coagulation factor Xa inhibitor, is used potentially for the treatment of septic shock.

α-Melanocyte-stimulating hormone (α-MSH) is a 13-amino acid peptide hormone produced by post-translational processing of proopiomelanocortin (POMC) in the pituitary gland, as well as in keratinocytes, astrocytes, monocytes, and gastrointestinal cells.1It is an agonist of melanocortin receptor 3 (MC3R) and MC4R that induces cAMP production in Hepa cells expressing the human receptors (EC50s = 0.16 and 56 nM, respectively).2α-MSH (100 pM) reducesS. aureuscolony formation andC. albicansgerm tube formationin vitro.3It inhibits endotoxin-, ceramide-, TNF-α-, or okadaic acid-induced activation of NF-κB in U937 cells.1α-MSH reduces IL-6- or TNF-α-induced ear edema in mice.4It also prevents the development of adjuvant-induced arthritis in rats and increases survival in a mouse model of septic shock. Increased plasma levels of α-MSH are positively correlated with delayed disease progression and reduced death in patients with HIV.1 1.Catania, A., Airaghi, L., Colombo, G., et al.α-melanocyte-stimulating hormone in normal human physiology and disease statesTrends Endocrinol. Metab.11(8)304-308(2000) 2.Miwa, H., Gantz, I., Konda, Y., et al.Structural determinants of the melanocortin peptides required for activation of melanocortin-3 and melanocortin-4 receptorsJ. Pharmacol. Exp. Ther.273(1)367-372(1995) 3.Cutuli, M., Cristiani, S., Lipton, J.M., et al.Antimicrobial effects of a-MSH peptidesJ. Leukoc. Biol.67(2)233-239(2000) 4.Lipton, J.M., Ceriani, G., Macaluso, A., et al.Antiiinflammatory effect of the neuropeptide a-MSH in acute, chronic, and systemic inflammationAnn. N.Y. Acad. Sci.25(741)137-148(1994)

Neuromedin U (NMU) is a neuropeptide first demonstrated to drive smooth muscle contraction.1Translated as a 174 amino acid propeptide, NMU is cleaved to different lengths in different animals. It has diverse receptor-mediated rolesin vivo, as it regulates feeding, vasoconstriction, nociception, and bone remodeling and contributes to obesity, cancer and septic shock.2,2NMU-25 is the active form of NMU in humans. It binds with high affinity to receptors on human left ventricle and coronary artery (KDs = 0.26 and 0.11 nM, respectively), eliciting endothelium-independent vasoconstriction.3NMU-25 also suppresses glucose-stimulated insulin secretion in human islets, and this effect is lost in NMU R165W mutants, resulting in early-onset obesity.4 1.Mitchell, J.D., Maguire, J.J., and Davenport, A.P.Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin SBritish Journal of Pharmacology15887-103(2009) 2.Greenwood, H.C., Bloom, S.R., and Murphy, K.G.Peptides and their potential role in the treatment of diabetes and obesityRev.Diabet.Stud.8(3)355-368(2011) 3.Mitchell, J.D., Maguire, J.J., Kuc, R.E., et al.Expression and vasoconstrictor function of anorexigenic peptides neuromedin U-25 and S in the human cardiovascular systemCardiovascular Research81353-361(2009) 4.Alfa, R.W., Park, S., Skelly, K.R., et al.Suppression of insulin production and secretion by a decretin hormoneCell Metabolism21(2)323-333(2015)

M62812是一种 TLR4抑制剂，可在 HEK239细胞中抑制 LPS 诱导的NF-κB 活化。

Protein conjugates in tissue regeneration 3 (PCTR3) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid . DHA is oxidized to 16S,17S-epoxy-protectin, which is converted to PCTR1 by glutathione S-transferase and to PCTR2 and PCTR3 via peptidases. PCTR3 is found in infected mouse spleens and resolving exudate as well as isolated human spleen and septic plasma. It is also found in both M1 and M2 macrophages differentiated from isolated human monocytes.

LL-37 is a cationic and α-helical antimicrobial peptide expressed in human bone marrow, testis, granulocytes, and gingival epithelium and is upregulated in psoriatic lesions. It inhibits growth of Gram-positive E. coli D21 and Gram-negative B. megatarium in a concentration-dependent manner and LL-37 expression is induced in A549 epithelial cells, alveolar macrophages, neutrophils, and monocyte-derived macrophages following M. tuberculosis infection. LL-37 binds sheep erythrocytes coated with S. minnesota Re-LPS and induces agglutination with a minimal agglutinating concentration (MAC) of 12.1 μg/ml. It is a chemoattractant for, and can induce calcium mobilization in, human monocytes, neutrophils, and T cells that naturally express formyl peptide receptor-like 1 (FPRL1) and FPRL1-transfected HEK293 cells. LL-37 (10-15 μM) pretreatment of dengue virus type 2 (DENV-2) reduces its infectivity as well as levels of viral genomic RNA and NS1 antigen. In vivo, LL-37 inhibits cecal ligation and puncture-induced caspase-1 activation and pyroptosis of peritoneal macrophages, reduces levels of the inflammatory cytokines IL-1β, IL-6, and TNF-α, and improves survival in polybacterial septic mice.

FPL-65447 hydrochloride is a selective D1 receptor agonist that has potential for the acute treatment of renal and cardiac failure and of sepsis and septic shock.

NOS-IN-3 是一个强效的、选择性的由 imidamide 衍生的NOS 抑制剂，对iNOS 的IC50值为20 µM。 NOS-IN-3 不抑制eNOS，几乎没有毒性，可用于研究治疗可诱导亚型涉及的疾病，如感染性休克。

Ac-FEID-CMK 是一种有效的斑马鱼特异性GSDMEb 衍生肽抑制剂。Ac-FEID-CMK 可减轻感染性休克的死亡率和肾损伤。Ac-FEID-CMK 在体内可抑制焦亡，减轻败血性 AKI (急性肾损伤)。Ac-FEID-CMK 可抑制 caspy2 介导的非典型炎症小体通路。