PCSK9
- Known as:
- PCSK9
- Catalog number:
- Y213429
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PCSK9
Related genes to: PCSK9
- Gene:
- PCSK9 NIH gene
- Name:
- proprotein convertase subtilisin/kexin type 9
- Previous symbol:
- HCHOLA3
- Synonyms:
- NARC-1, FH3
- Chromosome:
- 1p32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-13
- Date modifiied:
- 2019-04-23
Related products to: PCSK9
Related articles to: PCSK9
- Lipoprotein(a) (Lp(a)) is an independent risk factor for atherosclerotic cardiovascular disease. Although proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors modestly reduce Lp(a) levels, evidence regarding their dose-dependent effects on patients with extremely high Lp(a) levels is limited. A 69-year-old woman was diagnosed with dyslipidemia because of high low-density lipoprotein cholesterol (LDL-C) levels (>180 mg/dL) and was initiated on atorvastatin at a dose of 10 mg/day. Two years later, she developed a myocardial infarction, and heterozygous familial hypercholesterolemia was subsequently diagnosed. Eight years later, despite achieving optimal LDL-C levels using high-intensity statin therapy, ezetimibe, and a half-dose of a PCSK9 inhibitor (evolocumab 140 mg monthly), her Lp(a) levels remained high. Up-titration of evolocumab from 140 mg monthly to 140 mg every two weeks resulted in a 34.7% reduction in Lp(a) levels; however, the value only decreased to 82.5 mg/dL. This case indicates a dose-dependent effect of PCSK9 inhibitor therapy on Lp(a) reduction; however, the magnitude of lowering may be insufficient in patients with extremely high baseline Lp(a) levels. - Source: PubMed
Publication date: 2026/03/23
Suzuki NobuakiKishi Hisako - Lipoprotein(a) [Lp(a)] is a causal contributor to atherosclerotic cardiovascular disease (ASCVD). While no therapies are currently approved solely for lowering Lp(a), subgroup analyses suggest that individuals with elevated Lp(a) may gain added benefit from intensive lipid-lowering strategies. No prior meta-analysis has compared evolocumab, alirocumab, inclisiran, lerodalcibep, and enlicitide in their Lp(a)-lowering efficacy. We aimed to determine whether PCSK9-targeted therapies differ significantly in Lp(a) reduction, or whether agent selection can be guided primarily by other factors such as dosing frequency, cost, and patient preference. - Source: PubMed
Publication date: 2026/04/01
Mulligan Martin DGandhi Rahul SVishwakarma RishabhBhattacharya Romit - Cascade screening (CS) for familial hypercholesterolemia (FH) has been found to be cost-effective in many published studies. However, most existing studies (i) ignored or overstated first-degree relative (FDR) participation rate (as 60-100 %), (ii) did not consider novel and expensive therapies, e.g. PCSK9 inhibitors (PCSK9i), and (iii) were conducted outside of Asia. This study, conducted in Singapore, where FDR participation rate is about 25 % among probands who have known pathogenic variants, aims to identify drivers of cost-effectiveness of CS protocols for FH. - Source: PubMed
Publication date: 2025/07/12
Lou JingChong Kok JoonPek Sharon Li TingBylstra YasminDrum Chester LeeLim Weng KhongWang YiYeo Khung KeongTavintharan SubramaniamWee Hwee-Lin - Low-density lipoprotein cholesterol (LDL-C) is a key modifiable risk factor for atherosclerotic cardiovascular (CV) disease in patients with acute coronary syndrome (ACS). While high-intensity statins are foundational, many patients fail to reach guideline-recommended targets, leaving a high residual risk during the early post-ACS phase. Evidence from EVOPACS and EVACS trials demonstrates that early in-hospital proprotein convertase subtilisin/kexin type 9 inhibitor (PCSK9i) initiation achieves rapid, intensive LDL-C lowering, with over 90% of patients attaining targets of ≤1.4 mmol/L by discharge. Furthermore, the PACMAN-AMI and HUYGENS trials confirm that PCSK9i therapy promotes plaque regression and stabilisation by increasing fibrous cap thickness and reducing lipid-rich necrotic core content. Meta-analyses indicate significant reductions in major adverse CV events and ACS-related hospitalisations within 6-18 months. Early PCSK9i integration offers a potent, safe strategy to bridge lipid management gaps and optimize secondary prevention outcomes in high-risk populations, including those in India. - Source: PubMed
Publication date: 2026/04/20
Goel Pravin KKapoor AdityaJain Kala JeetenderThachathodiyl RajeshReddy VikasGuleria VivekBhalla NeerajSasidharan Shyam - Remnant cholesterol (RC) is increasingly recognized as an independent contributor to coronary heart disease (CHD) risk beyond low-density lipoprotein cholesterol (LDL-C). However, its causal roles, genetic determinants, tissue-specific regulation, and relevance across ancestrally diverse populations remain incompletely characterized. - Source: PubMed
Publication date: 2026/04/20
Han GuiyuanLei Chon LokShi YuGao JiajiaLiu XiaoyingPeng KeCai YunpengHoi Pui ManLi Yichong