CKMM Blocking Peptide
- Known as:
- CKMM Blocking Peptide
- Catalog number:
- 33r-9549
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- CKMM Blocking Peptide
Related genes to: CKMM Blocking Peptide
- Gene:
- CKM NIH gene
- Name:
- creatine kinase, M-type
- Previous symbol:
- CKMM
- Synonyms:
- -
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-02-10
Related products to: CKMM Blocking Peptide
Related articles to: CKMM Blocking Peptide
- The Remote Food Photography Method (RFPM) accurately estimates energy intake in adults, but its validity in adolescents has yet to be tested. Given the low accuracy of self-reported dietary intake in adolescents, evaluating the validity of the RFPM in both controlled and free-living settings is crucial. - Source: PubMed
Publication date: 2026/07/25
Höchsmann ChristophDiktas Hanim EMyers Candice ADorling James LRood Jennifer CGreenway FrankChampagne Catherine MApolzan John WMartin Corby K - The recent standardization of diagnostic criteria and phenotyping for cardiovascular-kidney-metabolic (CKM) syndrome has increased attention to this multisystem disorder which arises from the interactions among metabolic dysfunction, chronic kidney disease, and cardiovascular disease. The food inflammation index (FII) quantifies diet-induced inflammation and evaluates individuals' susceptibility to inflammatory-mediated health outcomes. However, the mechanisms linking FII derived dietary inflammation to CKM syndrome progression, especially the triglyceride-glucose (TyG) index's mediating role, remain unclear. This study aimed to investigate the association between FII and advanced CKM syndrome and evaluate the mediating role of TyG index. This study used a two-phase design to determine the dose-response relationship between FII and advanced CKM syndrome (stages 3 or 4) and to assess the TyG index's contribution in this link through mediation analysis. Data obtained from the 1999 to 2018 surveys were analyzed, and 20,151 participants were included in the analysis. CKM syndrome staging was done per established criteria, with advanced CKM as stage 3 or 4. Multivariate weighted logistic regression evaluated the association between FII and advanced CKM syndrome, with the TyG index as a mediator. The prevalence of advanced CKM syndrome was 17.37%. FII was significantly associated with advanced CKM stages (odds ratio = 1.03, 95% confidence interval = 1.01-1.04, P < .001), and this association was partially mediated by the TyG index (proportion mediated = 12.52%, 95% confidence interval = 7.25%-25.48%, P < .001). Higher FII levels were associated with an increased risk of advanced CKM syndrome, suggesting that FII may serve as a useful marker for prevention and early detection. The TyG index partially mediated the relationship between FII and advanced CKM syndrome. Future longitudinal studies are warranted to confirm these findings and explore potential interventions targeting dietary inflammation. - Source: PubMed
Fang BinquanLin JunjieLi XuanXu JiaminZheng MiaoJiang ZiyingZheng WeijunChen RuchengChen Cheng - Older adults are vulnerable to adverse drug reactions due to multimorbidity, frailty and polypharmacy. In those with cardiovascular-kidney-metabolic (CKM) syndrome, CKM-related multi-organ burden may further alter drug disposition and elevate risk. Metoprolol exposure varies widely among individuals, and higher plasma concentrations have been associated with falls in prior studies. We aimed to develop a population pharmacokinetic (PopPK) model of metoprolol in older Chinese patients with CKM syndrome using real-world data, identify key covariates affecting clearance, and perform model-based dose simulations. The PopPK analysis included sparse real-world data from 42 older adults (60-93 years) receiving immediate-release metoprolol tartrate. Candidate covariates included demographics, genetic polymorphism, laboratory variables, comorbidities, frailty phenotype, SARC-F score, age-adjusted Charlson Comorbidity Index, CKM stage and CKMS-BAG score. Model-based simulations were conducted across predefined genotype- and disease-burden strata to evaluate dosing scenarios against literature-based thresholds. Metoprolol pharmacokinetics were adequately described by a one-compartment model with first-order absorption and elimination. The rs1065852 T/T genotype and a high CKMS-BAG score (> 11) were associated with lower apparent clearance (CL/F), resulting in approximately 32% and 30% reductions in CL/F, respectively, and reduced interindividual variability in CL/F from 46.9% to 39.9%. Simulations identified subgroup-specific dosing regimens that maintained steady-state trough concentrations within a literature-derived range. In older Chinese patients with CKM syndrome, rs1065852 and CKM-related burden influenced metoprolol clearance and accounted for a considerable part of the observed variability between individuals. This study provides a model-informed framework for exposure-threshold-based dose stratification. Prospective validation with clinical outcomes and comprehensive CYP2D6 genotyping is warranted. - Source: PubMed
Chai HaodiSia Jie En ValerieHu DingyuanJia YunshuHu SuiyuanWu XinyiLiu DongyangLai XuanCui Cheng - Although creatine has a recognized role during gestation, there is still little information about multiple pregnancies. Especially in small ruminants, these pregnancies increase nutritional needs and the incidence of pre- and postpartum metabolic or reproductive pathologies. Thus, the main objective of this study was to address this gap by providing information on the impact of dietary supplementation with the creatine precursor guanidinoacetic acid (GAA) on the maternal-fetal response during late gestation in twin-bearing ewes. - Source: PubMed
Publication date: 2026/07/09
de Freitas Alves Bruna VitóriaCavalcanti Camila MunizConde Alfredo José HerreraCesar Larissa Fernandes Baiada Costa Sousa Martade Sena Jhennyfe NobreMiguel Yohana Huichoda Silva Pereira Fernando FelipeTeixeira Louhanna Pinheiro RodriguesÑaupas Lucy Vanessa Sulcada Silva Ana Flávia BezerraRodrigues Ana Paula RibeiroFernandes César Carneiro LinharesAlves Juliana Paula MartinsTeixeira Dárcio Ítalo AlvesRondina Davide - Cardiovascular-kidney-metabolic (CKM) syndrome, formally defined by the American Heart Association in 2023, affects approximately 90% of US adults, who meet criteria for stage 1 or higher. The rapid convergence of multiple drug classes on CKM pathways-SGLT2 inhibitors, finerenone, GLP-1 receptor agonists, ARNI, and interleukin-directed therapies-has created an urgent need for pharmacologically grounded frameworks that guide drug selection, interpret biomarker responses, and monitor target engagement across interconnected organ systems. This review proposes a three-dimensional biomarker-guided approach to precision pharmacotherapy in CKM syndrome. In the organ-specific dimension, we map key biomarkers to their corresponding drug targets and elucidate the molecular mechanisms underlying drug-biomarker interactions: SGLT2 inhibitors attenuate myocardial injury through metabolic substrate shifting toward ketone body utilization and, based on preclinical evidence, NHE1 inhibition; neprilysin selectivity of sacubitril/valsartan explains the differential natriuretic peptide response; and tubuloglomerular feedback mediates the renoprotective hemodynamic effects of SGLT2 inhibitors. In the pathway-specific dimension, we identify cross-system biomarkers-hs-CRP, IL-6, galectin-3, GDF-15, and FGF21-that reveal shared druggable targets spanning the IL-1β/NLRP3 inflammasome axis (canakinumab, colchicine), IL-6 trans-signaling (ziltivekimab), and FGF21/β-klotho metabolic signaling. In the temporal dimension, we demonstrate how serial biomarker trajectories serve as pharmacodynamic readouts that distinguish therapeutic drug effects from disease progression, including the initial eGFR dip with SGLT2 inhibitors and natriuretic peptide changes during combination therapy. Central to this framework is the concept of "pharmacological phenotyping"-using multi-biomarker panels to define drug-responsive pathophysiological states that directly inform therapeutic selection, analogous to companion diagnostics in oncology. We further present a comprehensive drug-biomarker interaction matrix with pharmacological rationale and analyze the emerging drug development pipeline, including RNA-based Lp(a) therapeutics, FGF21 analogues, galectin-3 inhibitors, and in vivo CAR-T anti-fibrotic approaches. This framework provides a practical roadmap for biomarker-guided precision pharmacotherapy in CKM syndrome. - Source: PubMed
Publication date: 2026/07/23
Li YafengSong WenzhuHuan ChengyuXu KemanSun JuanZhen XinOuyang HuaTang HairongFan QiuxiaZhi WenqiangChai YuanminLi RuilinWang HongYang Xiaofeng