lipid 5

Lipid 5 is an amino lipid compound that demonstrates proficient mRNA delivery in rodent and primate models, displaying favorable pharmacokinetics and minimal toxicity.

LNP Lipid-5 (化合物 Lipid 2) 是一种可电离的氨基脂质。LNP Lipid-5 适用于脂质纳米颗粒 (LNP) 的制备。

3D-Monophosphoryl Lipid A-5 (free acid) 作为一种有效的TLR激动剂，常用于疫苗中作为佐剂，用以提升疫苗的免疫原性。

3D-Monophosphoryl Lipid A-5 (3D-MPLA-5) triethylamine 作为一种TLR激动剂，主要用作疫苗佐剂，其主要功能是提升疫苗的免疫原性。

3D-Monophosphoryl Lipid A-5 (3D-MPLA-5) 是一种TLR激动剂，用于作为疫苗佐剂，以提高疫苗的免疫原性。

Sphingosine-1-phosphate (S1P) 是 S1P1-5 受体 (S1P1-5 receptors) 的激动剂和 GPR3、GPR6、GPR12 的配体。Sphingosine-1-phosphate 是细胞内的第二信使，动员 Ca2+ 作为 G 蛋白偶联受体的细胞外配体。Sphingosine-1-phosphate 是由鞘磷脂或其他膜磷脂生成的重要脂质介质。

Berberine (Umbellatine) 属于生物碱类天然产物，可以激活 AMPK、抑制 DNA 拓扑异构酶、诱导 ROS 生成。Berberine 具有抗肿瘤、抗菌、降血糖、降血脂等生物学活性。

Peimisine (Ebeiensine) 非竞争性拮抗气管平滑肌 M 受体，抑制 Ach 引起的平滑肌收缩。它兴奋 β 受体和拮抗内钙释放，促进一氧化氮释放，可舒张气管平滑肌，有平喘作用。

Bragsin2 (6-methoxy-5-nitro-2-(trifluoromethyl)chromen-4-one) 是非竞争性的核苷酸交换因子 BRAG2选择性抑制剂，其 IC50值为 3 μM。它能够结合到 BRAG2 的 PH 结构域和磷脂双分子层的界面处，使 BRAG2 无法激活磷脂化的 Arf GTPase。它能够影响乳腺癌干细胞。

7α-Hydroxycholesterol 是一种由酶促氧化和非酶促氧化形成的胆固醇氧化物，可用作脂质过氧化的生物标志物。

Photosensitizer-5是一种在生物医学领域内具有重要应用的光敏剂。该化合物对HeLa和HepG2细胞线显示出显著的细胞毒性，其IC50值分别为10.4 nM和6.9 nM。此外，Photosensitizer-5能诱导脂质过氧化以及通过铁非依赖性细胞死亡途径引发细胞死亡，这在HeLa荷瘤小鼠模型中显示出抑制肿瘤的潜力。

Ferroptosisinducer-4 (Compound 5) 作为一种有效的铁死亡 (Ferroptosis) 诱导剂，其分子结构特征为在 sn-2 位点具有末端双键的磷脂。该化合物对 HT-1080 细胞线显示出显著的细胞毒性，具有 18 μM 的 IC50 值。其毒性作用主要通过末端双键催化的脂质过氧化和细胞膜氧化损伤进行。Ferroptosisinducer-4 在研究铁死亡调控机制中有重要应用。

Ionizable Lipid 4, 一种阳离子脂质，是在过氧化氢诱导下CA-lipid 5重排的产物。

PPARγ-IN-5 (Compound A3) 是一种PPARγ抑制剂，在肝细胞中有效抑制脂质累积，并在 HepG2 细胞（400 µM）条件下无显著细胞毒性。PPARγ-IN-5 可用于研究非酒精性脂肪性肝病。

HDAC11-IN-2 (compound B6) 是一种针对组蛋白去乙酰化酶 11 (Histone Deacetylase 11, HDAC11) 的高度选择性抑制剂。其抑制HDAC11和HDAC8的IC50值分别为51.1 ×10^-3μM和5 μM。HDAC11-IN-2 能抑制新生脂肪生成 (DNL) 并促进脂肪酸氧化，从而减轻MASLD小鼠的肝脏脂质积累和病理症状。通过抑制HDAC11，该化合物增强AMPKα1在Thr172位点的磷酸化，从而调节肝脏的新生脂肪生成和脂肪酸氧化。

SST-02 is a potent cationic lipid for siRNA-Lipid Nanoparticles. SST-02 possesses a simple chemical structure and is synthesized just in one step. SST-02 showed an ID50 of 0.02 mg kg in the factor VII (FVII) model. Rats administered with 3 mg kg of SST-02

1-Stearoyl-3-oleoyl-rac-glycerol is a diacylglycerol that contains stearic acid at the sn-1 position and oleic acid at the sn-3 position. Intermittent fasting decreases skeletal muscle and hepatic levels of 1-stearoyl-3-oleoyl-rac-glycerol in New Zealand obese (NZO) mice.1 The concentration of 1-stearoyl-3-oleoyl-rac-glycerol decreases from 4.59 to 1.88% during the dry-curing process of Iberian ham.2References1. Baumeier, C., Kaiser, D., Heeren, J., et al. Caloric restriction and intermittent fasting alter hepatic lipid droplet proteome and diacylglycerol species and prevent diabetes in NZO mice. Biochim. Biophys. Acta 1851(5), 566-576 (2015).2. Narváez-Rivas, M., Vicario, I.M., Constante, E.G., et al. Changes in the concentrations of free fatty acid, monoacylglycerol, and diacylglycerol in the subcutaneous fat of Iberian ham during the dry-curing process. J. Agric. Food Chem. 55(26), 10953-10961 (2007). 1-Stearoyl-3-oleoyl-rac-glycerol is a diacylglycerol that contains stearic acid at the sn-1 position and oleic acid at the sn-3 position. Intermittent fasting decreases skeletal muscle and hepatic levels of 1-stearoyl-3-oleoyl-rac-glycerol in New Zealand obese (NZO) mice.1 The concentration of 1-stearoyl-3-oleoyl-rac-glycerol decreases from 4.59 to 1.88% during the dry-curing process of Iberian ham.2 References1. Baumeier, C., Kaiser, D., Heeren, J., et al. Caloric restriction and intermittent fasting alter hepatic lipid droplet proteome and diacylglycerol species and prevent diabetes in NZO mice. Biochim. Biophys. Acta 1851(5), 566-576 (2015).2. Narváez-Rivas, M., Vicario, I.M., Constante, E.G., et al. Changes in the concentrations of free fatty acid, monoacylglycerol, and diacylglycerol in the subcutaneous fat of Iberian ham during the dry-curing process. J. Agric. Food Chem. 55(26), 10953-10961 (2007).

(±)10-HDHA is an autoxidation product of docosahexaenoic acid (DHA) in vitro.[1][2] It is also produced from incubations of DHA in rat liver, brain, and intestinal microsomes.[3][4][5] (±)10-HDHA is a potential marker of oxidative stress in brain and retina where DHA is an abundant polyunsaturated fatty acid. Reference：[1]. VanRollins, M., and Murphy, R.C. Autooxidation of docosahexaenoic acid: Analysis of ten isomers of hydroxydocosahexaenoate. J. Lipid Res. 25(5), 507-517 (1984).[2]. Reynaud, D., Thickitt, C.P., and Pace-Asciak, C.R. Facile preparation and structural determination of monohydroxy derivatives of docosahexaenoic acid (HDoHE) by α-tocopherol-directed autoxidation. Anal. Biochem. 214(1), 165-170 (1993).[3]. VanRollins, M., Baker, R.C., Sprecher, H., et al. Oxidation of docosahexaenoic acid by rat liver microsomes. J. Biol. Chem. 259(9), 5776-5783 (1984).[4]. Yamane, M., Abe, A., and Yamane, S. High-performance liquid chromatography-thermospray mass spectrometry of epoxy polyunsaturated fatty acids and epoxyhydroxy polyunsaturated fatty acids from an incubation mixture of rat tissue homogenate. J. Chromatogr. 652(2), 123-136 (1994).[5]. Kim, H.Y., Karanian, J.W., Shingu, T., et al. Sterochemical analysis of hydroxylated docosahexaenoates produced by human platelets and rat brain homogenate. Prostaglandins 40(5), 473-490 (1990).

4-hydroxy Nonenal is a lipid peroxidation product derived from oxidized ω-6 polyunsaturated fatty acids such as arachidonic acid and linoleic acid. [1] [2] It exhibits various biological activities such as cytotoxicity, growth inhibiting activity, genotoxicity, and chemotactic activity and has been widely used as a marker of lipid peroxidation.[1][2][3] 4-oxo-2-Nonenal is a more recently identified product of lipid peroxidation.[4][5][6] It actively modifies histidine and lysine residues on proteins and causes protein cross-linking. [7][8] 4-oxo-2-Nonenal also modifies 2’-deoxyguanosine, further implicating lipid peroxidation in mutagenesis and carcinogenesis.[4]

MTP 131 acetate 是一种小的线粒体靶向四肽。

Palmitic acid-13C is intended for use as an internal standard for the quantification of palmitic acid by GC- or LC-MS. Palmitic acid is a 16-carbon saturated fatty acid. It comprises approximately 25% of human total plasma lipids.1 It increases protein levels of COX-2 in RAW 264.7 cells when used at a concentration of 75 μM.2 Palmitic acid is involved in the acylation of proteins to anchor membrane-bound proteins to the lipid bilayer.2,3,4,5,6 |1. Santos, M.J., López-Jurado, M., Llopis, J., et al. Influence of dietary supplementation with fish oil on plasma fatty acid composition in coronary heart disease patients. Ann. Nutr. Metab. 39(1), 52-62 (1995).|2. Lee, J.Y., Sohn, K.H., Rhee, S.H., et al. Saturated fatty acids, but not unsaturated fatty acids, induced the expression of cyclooxygenase-2 mediated through toll-like receptor 4. J. Biol. Chem. 276(20), 16683-16689 (2001).|3. Dietzen, D.J., Hastings, W.R., and Lublin, D.M. Caveolin is palmitoylated on multiple cysteine residues. Palmitoylation is not necessary for localization of caveolin to caveolae. J. Biol. Chem. 270(12), 6838-6842 (1995).|4. Robinson, L.J., and Michel, T. Mutagenesis of palmitoylation sites in endothelial nitric oxide synthase identifies a novel motif for dual acylation and subcellular targeting. Proc. Nat. Acad. Sci. USA 92(25), 11776-11780 (1995).|5. Topinka, J.R., and Bredt, D.S. N-terminal palmitoylation of PSD-95 regulates association with cell membranes and interaction with K+ channel Kv1.4. Neuron 20(1), 125-134 (1998).|6. Miggin, S.M., Lawler, O.A., and Kinsella, B.T. Palmitoylation of the human prostacyclin receptor. Functional implications of palmitoylation and isoprenylation. J. Biol. Chem. 278(9), 6947-6958 (2003).

Palmitic acid-13C is intended for use as an internal standard for the quantification of palmitic acid by GC- or LC-MS. Palmitic acid-13C contains 13C at the C2 position and has been used in the study of free fatty acid incorporation into phospholipid fatty acids in soil microbes.1 Palmitic acid is a 16-carbon saturated fatty acid. It comprises approximately 25% of human total plasma lipids.2 It increases protein levels of COX-2 in RAW 264.7 cells when used at a concentration of 75 μM.3 Palmitic acid is involved in the acylation of proteins to anchor membrane-bound proteins to the lipid bilayer.3,4,5,6,7

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]