non-lipid

SKI V is a potent and noncompetitive non-lipid sphingosine kinase (SPHK; SK) inhibitor (GST-hSK,IC50 : 2 μM), and is a PI3K inhibitor(hPI3k,IC50 : 6 μM), induces apoptosis and has antitumor activity

DBIBB is a non-lipid agonist of specific lysophosphatidic acid (LPA2) type 2 G-protein-coupled receptor. It is a potentially active molecule for the treatment of acute radiation syndrome caused by high intensity gamma rays on hematopoietic and gastrointestinal systems. It is an intermediate in organic synthesis and drug research. DBIBB can be used to prepare various compounds that reduce gastrointestinal radiation syndrome, increase intestinal crypt survival and intestinal cell proliferation, and reduce cell apoptosis.

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

timcodar is a non-FKBP12 binding macrolide derivative that is an efflux pump inhibitor with antimicrobial activity, inhibition of lipid accumulation, inhibition of Mycobacterium tuberculosis, and can be used in the study of obesity. timcodar is a non-FKBP12 binding macrolide derivative with antimicrobial activity.

Triton X-100 is a non-denaturing detergent that solubilizes lipid membranes. Triton X-100 is commonly used in laboratories and is applied to vaccines at different stages of the manufacturing process. Triton X-100 is listed as an excipient in certain vaccines including split virus influenza vaccines. Triton X-100 is a nonionic surfactant [1] [2].

Triacsin C (WS 1228A) from Streptomyces aureofaciens is a differential inhibitor of arachidonic acid coenzyme A synthetase and non-specific long-chain acyl-coenzyme A synthetase, with anti-atherosclerotic activity, inhibition of ACSL activity, and inhibition of the accumulation of TAGs into lipid droplets (LDs).Triacsin C has been used to study rotavirus infection and Alzheimer;s disease. Triacsin C is used to study rotavirus infection and Alzheimer;s disease.

Bragsin2 (6-methoxy-5-nitro-2-(trifluoromethyl)chromen-4-one) is a hydration-resistant cell penetrant, selective and non-competitive inhibitor of Afr guanine nucleotide exchange factor BRAG2 that inhibits Arf GTPase activation, with an IC50 of 3 μM. Bragsin2 binds at the interface between the pleckstrin homology domain of BRAG2 and the lipid bilayer, leading BRAG2 unable to activate lipidated Arf GTPase.

Cetaben, a PPARα-independent peroxisome proliferator, is a non-fibrotic lipid-lowering drug that effectively reduces cholesterol and triglyceride concentrations.

DOPE (DOPE) is a neutral helper lipid for cationic liposomes.It is used in combination with cationic phospholipids to increase efficiency during DNA transfection studies as a non-viral method of gene delivery.

7α-Hydroxycholesterol, a cholesterol oxide formed through both enzymatic and non-enzymatic oxidation, can serve as a biomarker for lipid peroxidation.

PCSK9-IN-29 serves as a lipid-lowering agent that enhances the expression of low-density lipoprotein receptor (LDLR) protein and reduces PCSK9 protein expression in hepG2 cells. Additionally, in crab-eating macaques on a high-fat diet, it lowers serum LDL-C, TC, and liver enzyme ALT levels, reduces body weight and fat, and boosts bone mineral content. PCSK9-IN-29 is useful for studies involving non-alcoholic fatty liver disease and obesity.

ABCA1 inducer 1, a non-lipid inducer of ABCA1, enhances ABCA1 expression in E3/4FAD mice expressing human APOE 3/4, augments the lipidation of apolipoprotein (APOE), and reverses various Alzheimer's disease (AD) phenotypes without increasing triglycerides.

SET-171 is a JNK (c-Jun N-terminal kinase) inhibitor that exhibits significant anticancer activity by suppressing the expression of hepatic pyruvate kinase (PKL) and offers potential in regulating lipid metabolism. In antitumor studies, SET-171 shows notable cytotoxicity against human liver cancer cell lines HepG2 and Huh7, with IC50 values of 8.82 μM and 2.97 μM, respectively. Additionally, in research related to non-alcoholic fatty liver disease (NAFLD), SET-171 significantly reduces triglyceride (TAG) levels and inhibits the expression of proteins associated with steatosis. This compound holds promise for hepatocellular carcinoma (HCC) and NAFLD research.

D-Psicose (D-Allulose) is an orally active rare sugar. It effectively inhibits p38-MAPK phosphorylation and MCP-1 expression, while blocking the AGEs/RAGE/NF-kappaB signaling pathway. D-Psicose demonstrates significant bioactivity in research involving pancreatic beta-islet protection, hyperglycemia improvement, lipid metabolism regulation, and the mitigation of high-fat diet-induced non-alcoholic fatty liver disease (NAFLD).

18:0 Diether PC (1,2-Di-O-octadecyl-sn-glycero-3-phosphocholine) is a glycerophospholipid utilized as a non-hydrolyzable ether lipid in chlorophyll-containing vesicles.

PPARγ-IN-5 (Compound A3) is an inhibitor of PPARγ. In liver cells, it reduces lipid accumulation and shows no significant cytotoxicity in HepG2 cells at a concentration of 400 µM. PPARγ-IN-5 is applicable for research on non-alcoholic fatty liver disease.

ABCA1 inducer 2 is a non-lipogenic inducer of ABCA1. It increases the expression of ABCA1 by targeting the LXR pathway, thereby reducing lipid accumulation induced by ox-LDL and inhibiting foam cell formation. ABCA1 inducer 2 holds potential as an anti-atherosclerotic agent.

ACC-IN-1 (Compound B1) is an allosteric inhibitor of acetyl-CoA carboxylase (ACC). It targets ACC to regulate lipid metabolism, potentially improving liver steatosis and inflammation associated with non-alcoholic steatohepatitis (NASH).

TMX-4102 is a highly selective binder of phosphatidylinositol 5-phosphate 4-kinase Type II gamma (PIP4K2C). It demonstrates binding activity to PIP4K2C with a dissociation constant (KD) of 0.45 nM, and does not significantly affect other lipid and non-lipid kinases. By specifically binding to PIP4K2C, TMX-4102 regulates its scaffold function rather than its enzymatic activity. TMX-4102 serves as a tool molecule for studying the biological functions and potential therapeutic value of PIP4K2C.

TBPH exacerbates liver steatosis, inflammation, and fibrosis in non-alcoholic steatohepatitis (NASH) mouse models. It induces phospholipid metabolism disorders, reducing cardiolipin (CL) and phosphatidylserine (PS) levels. TBPH impairs endoplasmic reticulum-mitochondria (ER-Mito) contact, leading to mitochondrial dysfunction. Additionally, TBPH causes lung injury through mitochondrial-derived ds-DNA-mediated inflammatory responses. TBPH is utilized to study the role of MFN2-mediated ER-Mito contact in lipid metabolism homeostasis.

TBPH is a brominated flame retardant that exacerbates hepatic steatosis, inflammation, and fibrosis in non-alcoholic steatohepatitis (NASH) mouse models. It disrupts phospholipid metabolism, reducing levels of cardiolipin (CL) and phosphatidylserine (PS). TBPH impairs endoplasmic reticulum-mitochondria (ER-Mito) contact, leading to mitochondrial dysfunction. Additionally, TBPH induces lung injury through a mitochondrial-derived ds-DNA mediated inflammatory response. It is also used to investigate the role of MFN2-mediated ER-Mito contact in lipid metabolism homeostasis.

DHODH-IN-33 is a selective DHODH inhibitor that exhibits potent activity against A549 cells (IC50 = 5.22 μM) and 5637 cells (IC50 = 3.03 μM). It induces autophagy-dependent ferroptosis, characterized by mitochondrial dysfunction, lipid peroxidation, and accumulation of ROS, without significant toxicity in vivo. The anticancer effect of DHODH-IN-33 is achieved through promoting autophagy-dependent degradation of dihydroorotate dehydrogenase. This compound can be used in studies related to non-small cell lung cancer and bladder cancer.

STAT3-IN-51 is a STAT3 inhibitor that binds directly to the SH2 domain of STAT3. This compound induces apoptosis, ferroptosis, and immunogenic cell death (ICD), enhancing antitumor immunity. It suppresses STAT3 activation (phosphorylation, p-STAT3) and its downstream signaling, while prompting reactive oxygen species (ROS) generation, decreasing Bcl-2 expression, disrupting mitochondrial functions, inhibiting GPX4 activity, and promoting lipid peroxidation. STAT3-IN-51 is applicable in research on colorectal cancer, breast adenocarcinoma, non-small cell lung cancer (NSCLC), and cisplatin-resistant lung adenocarcinoma.

5-CNAC is an orally effective absorption enhancer with no inherent pharmacological activity. It significantly increases the gastrointestinal absorption efficiency of co-administered drugs (such as salmon calcitonin). By reversibly binding to peptide drugs in a non-covalent manner, 5-CNAC protects them from enzymatic degradation in the gastrointestinal tract and enhances lipid solubility, facilitating passive transepithelial transport without compromising intestinal epithelial integrity. It is useful in research as an adjuvant for oral peptide administration.