CETP
- Known as:
- CETP
- Catalog number:
- Y214494
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CETP
Related genes to: CETP
- Gene:
- CETP NIH gene
- Name:
- cholesteryl ester transfer protein
- Previous symbol:
- -
- Synonyms:
- BPIFF
- Chromosome:
- 16q13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-17
Related products to: CETP
Active Recombinant Human CETPActive Recombinant Human CETPActive Recombinant Human CETPActive Recombinant Human CETP proteinsActive Recombinant Human CETP proteinsActive Recombinant Human CETP proteinsAnserine Cholesteryl Ester Transfer Protein Elisa Kit (CETP)Anserine anti - Cholesteryl Ester Transfer Protein Elisa Kit (CETP)Anti CETP Human, Monoclonal Antibody (Clone No. CETP_4)Anti CETP Human, Monoclonal Antibody (Clone No. CETP_4) Cholesteryl ester tranfer protein (CETP) is one of the lipid transfer proteins, which mediates the transfer of cholesteryl ester (CE), triglycerAnti CETP Human, Monoclonal Antibody (Clone No. CM5, a_27)Anti CETP Human, Monoclonal Antibody (Clone No. CM5, a_27) This monoclonal antibody, specifically recognizes SDS_treated CETP, is applicable to immunostaining on nitrocellulose membrane.anti-CETPanti-CETPAnti-CETP Antibody Related articles to: CETP
- Hypercholesterolemia is a major risk factor for cardiovascular disease, necessitating the development of effective and safe lipid-lowering interventions. This study evaluated the antihypercholesterolemic effects of KGC11, a red ginseng oil obtained via supercritical fluid extraction, using both HepG2 cells and a high-fat/high-cholesterol diet-induced hypercholesterolemic rat model. KGC11 treatment significantly improved serum and hepatic lipid profiles, reduced markers of liver injury, and enhanced fecal cholesterol excretion. At the molecular level, KGC11 modulated the expression of key genes involved in cholesterol biosynthesis (3-hydroxy-3-methylglutaryl-CoA reductase), esterification (acyl-CoA:cholesterol acyltransferase), transport (CETP, LPL), and catabolism (LCAT, cholesterol 7α-hydroxylase). Collectively, these findings suggest that KGC11 may serve as a safe, food-derived functional ingredient with potential benefits for the management of hypercholesterolemia and related metabolic disorders. Further studies are warranted to elucidate its molecular mechanisms and to confirm its clinical efficacy. - Source: PubMed
Publication date: 2026/04/16
Park Soo-JeungLee MinheePark Seong-HooKim HyelimPark JiYeonKwon Han OlKim Jong HanLee Jeongmin - The statins remain the foundation of lipid management because they lower low-density lipoprotein cholesterol (LDL-C) and prevent cardiovascular events, and guidelines recommend stepwise intensification, often with ezetimibe first, when targets are not met or when intolerance limits dosing. This review introduces a mechanism-first, phenotype-guided framework that links add-on therapies to the dominant driver of residual risk, LDL-C, triglyceride-rich lipoproteins, elevated lipoprotein(a), or inherited dyslipidemia while integrating trial evidence with clinical practicality. Proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies remain the best-validated add-on for very high-risk patients. FOURIER and ODYSSEY OUTCOMES demonstrated event reduction with evolocumab or alirocumab on background statin therapy. For patients who cannot tolerate adequate statin doses, bempedoic acid provides liver-selective inhibition of adenosine triphosphate (ATP)-citrate lyase, and CLEAR Outcomes showed fewer major cardiovascular events in statin-intolerant populations. Inclisiran extends PCSK9 pathway suppression through hepatic small interfering RNA (siRNA) and enables durable LDL-C reduction with twice-yearly maintenance dosing, offering an adherence-oriented alternative while outcomes data mature. Angiopoietin-like protein 3 (ANGPTL3)-directed therapies (evinacumab and investigational RNAi agents such as zodasiran) lower atherogenic lipoproteins through largely LDL receptor independent biology. They expand options for refractory disease, including homozygous familial hypercholesterolemia. Apolipoprotein C-III (ApoC-III) inhibitors (olezarsen and plozasiran) drive large triglyceride reductions that can be decisive in severe hypertriglyceridemia and pancreatitis-prone syndromes. Next-generation cholesteryl ester transfer protein (CETP) inhibition (notably obicetrapib) has re-emerged as an oral strategy with substantial lipid effects as outcomes programs progress. High-dose eicosapentaenoic acid (EPA) (icosapent ethyl) has the clearest triglyceride-focused outcomes signal; REDUCE-IT showed significant ischemic event reduction in statin-treated patients with persistent hypertriglyceridemia. Early PCSK9 gene-editing is considered a potential one-time approach, though safety and durability concerns remain unresolved. Implementation remains rate-limiting. Costs, prior authorization, variable coverage, distribution, injection logistics, and adherence barriers delay initiation and erode persistence. Uninsured patients may face prohibitive out-of-pocket expenses without assistance pathways. - Source: PubMed
Publication date: 2026/03/26
Patel JayShah SamarthReddy AlaykaPrajapati DeepPandya AbhijitSawhney Sumit - This review examines whether high high-density lipoprotein cholesterol (HDL-C) is protective, harmful, or simply misleading in relation to atherosclerotic cardiovascular disease (ASCVD), with emphasis on recent mechanistic, epidemiologic, genetic, and trial evidence. - Source: PubMed
Publication date: 2026/04/07
Parini PaoloPedrelli Matteo - Cholesteryl ester transfer protein (CETP) is a crucial therapeutic target for combating cardiovascular disease (CVD) due to its strong influence in modulating high-density lipoprotein (HDL) levels. CETP is responsible for the bidirectional transfer of cholesteryl esters (CEs) and triglycerides (TGs) between different lipoprotein fractions. Although CETP encounters both these neutral lipid substrates when it penetrates deep into lipoprotein cores and can acquire either lipid, prior studies have examined its conformational space only in the presence of CEs or TGs individually. Here, we investigate the uncharacterised dynamics of CETP in heterogeneous lipid environments (CE-TG and TG-CE) using molecular dynamics simulations. Compared to the stable, homogeneous CE-bound state, the introduction of TG, particularly in mixed CE/TG configurations, induces significant structural instability and protein expansion. Mixed-lipid occupancy leads to elevated flexibility in critical lipoprotein-binding loops and the distortion of vital secondary structural elements. Furthermore, large-scale collective motion analyses reveal that heterogeneous binding forces CETP into aberrant, asymmetric, and hyper-twisted conformations. This disrupts the symmetric bending-twisting balance essential for efficient lipid exchange. Free energy landscapes confirm that the TGs within the mixed-lipid systems exhibit varied conformational states and adopt orientations that deviate from their reported parallel N-N orientation for lipid transfer through CETP. These findings suggest that the simultaneous presence of CE and TG imposes considerable conformational strain, fundamentally impairing CETP's lipid transport mechanism and offering novel mechanistic insights for future CETP-targeted therapeutics. - Source: PubMed
Publication date: 2026/04/08
Parthasarathy Bharath RajSenapati Sanjib - We assessed whether Tridax procumbens (TP) extracts could be used therapeutically against pancreatic cancer and remain nontoxic to normal cell types. The crude extract from TP (CETP) was fractionated using hexane, dichloromethane, and ethyl acetate to obtain fractions (NHF, DCMF, and EAF, respectively). The pancreatic ductal adenocarcinoma cell line (PANC-1) was cultured with (10, 20, 50, 100, and 250 μg/mL) dimethyl sulfoxide (DMSO) (control), CETP, and CETP-fractions for 24 or 48 h. As a normal cell type, we cultured E11.5d mouse pancreatic explants for five days before treating with the test samples (20 μg/mL) in DMSO for a further 48 h. Cytotoxicity assays (MTT and Live-Dead) were conducted, and the expression of cellular biomarkers, such as vimentin, Ki-67, p53, p21, and caspase-3, was evaluated. DCMF elicited PANC-1 cell death (IC = 23.1 μg/mL) compared to CETP (IC = 114.2 μg/mL). There were significant elevations in p53 (2.8-fold), caspase-3 (2.9-fold), catalase (4.0-fold), p21 (4.4-fold), and ALP (5.0-fold) proteins in DCMF-treated cells compared to control. DCMF significantly suppressed PNA and GST-pi (2.3-fold), Ki-67 (2.7-fold), and vimentin (10.8-fold) in PANC-1 cells relative to control. Also, DCMF induced Bcl-2 perinuclear staining and cytoplasmic translocation of APC in treated cells. Phenotype morphogenesis was observed in DCMF-treated embryonic pancreas with immunopositivity for insulin, vimentin, and amylase (1.3-fold), cytokeratin-7 (1.5-fold), PNA (1.9-fold), and glucagon (2.8-fold). In conclusion, Tridax procumbens appear to exert its anticancer effect via induction of apoptosis, antioxidant enzymes, and suppression of growth, proliferation, and invasiveness in PANC-1 cells without any observable toxicity on the normal embryonic pancreas. - Source: PubMed
Publication date: 2026/04/06
Samuel EkundayoEggleston IanTosh DavidOdunola Oyeronke