G6PD Blocking Peptide
- Known as:
- Glucose-6-phosphate dehydrogenase Blocking Peptide
- Catalog number:
- 33r-9850
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- G6PD Blocking Peptide
Ask about this productRelated genes to: G6PD Blocking Peptide
- Gene:
- G6PD NIH gene
- Name:
- glucose-6-phosphate dehydrogenase
- Previous symbol:
- -
- Synonyms:
- G6PD1
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: G6PD Blocking Peptide
Related articles to: G6PD Blocking Peptide
- A 23-month-old, 8-kg boy with known glucose-6-phosphate dehydrogenase (G6PD) deficiency presented with a coin lodged in the upper esophagus and required urgent rigid esophagoscopy under general anesthesia. Anesthetic management was planned to avoid drugs with oxidative potential and to minimize physiologic stressors that could contribute to hemolysis or methemoglobinemia. General anesthesia was performed using agents considered safe in patients with G6PD deficiency, with intraoperative management focused on maintaining normoxia using the lowest possible inspired oxygen concentration needed to maintain oxygen saturation above 95%, normothermia, and hemodynamic stability. The foreign body was removed without complications, and there were no clinical signs of hemolysis or methemoglobinemia during hospitalization. Postoperative monitoring included serial hemoglobin assessment and clinical surveillance for jaundice and dark urine for more than 24 hours, with no evidence of delayed hemolysis. A follow-up phone call at 72 hours confirmed that there were no symptoms. This case highlights a practical perioperative approach to emergent pediatric anesthesia in a patient with G6PD deficiency, emphasizing careful drug selection and proactive prevention and monitoring of oxidative triggers. - Source: PubMed
Publication date: 2026/05/11
Khaliq AliGrancaric NatasaGirshin MichaelMendonca RoniSuler Benjamin J - Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzymatic disorder of red blood cells, with particularly high prevalence in Sardinia, where it is strongly associated with favism. Public awareness remains incomplete and misconceptions persist-particularly regarding symptom onset from fava bean pollen or odors. This cross-sectional survey assessed G6PD self-reported deficiency, population knowledge, and persistence of false beliefs in Sardinia. A 16-item structured questionnaire was disseminated online (May-June 2025) to adults across diverse age groups and educational backgrounds. Among 536 respondents (74.25% female; 97.39% Sardinia residents), 43.47% of respondents self-reported as G6PD-deficient, a figure substantially above the expected population estimate of 8-15% and consistent with affected-network recruitment. Moreover, 49.07% self-reported as non-deficient, and 7.46% were unaware of their status. While 99.07% correctly identified fava bean ingestion as a trigger and 74.25% identified certain medications, 62.50% incorrectly attributed hazard to pollen inhalation and 25.93% to pea consumption. Only 3.92% reported a hemolytic crisis, whereas 25.93% reported feeling unwell after smelling beans or inhaling pollen. Family and friends (49.81%) and healthcare providers (42.16%) were the primary information sources; schools (25.75%) and online resources (14.55%) were underrepresented. Overall, 90.45% perceived public information as insufficient-uniformly across G6PD strata (χ = 0.09, = 0.955). Exploratory analyses suggested lower perceived information adequacy among younger respondents (Cochran-Armitage Z = 2.92, = 0.002) and, less robustly, among female respondents (χ = 3.90, = 0.048; borderline significance, unadjusted). Although recognition of fava bean ingestion as the principal dietary trigger is nearly universal, substantial gaps persist regarding non-ingestive exposures, less-recognized dietary triggers, and pharmacological risks. Perceived information insufficiency was independent of G6PD status but associated with younger age and female sex. Integrating targeted nutritional education into school curricula, primary care, and digital platforms is warranted for these priority groups and for G6PD-endemic populations worldwide. - Source: PubMed
Publication date: 2026/05/22
Serreli GabrieleMelis Maria PaolaGuerriero ClaudiaDeiana Monica - Adverse drug reactions (ADRs) remain a major public health issue, and genetic factors contribute importantly to interindividual variability in drug response. Pharmacogenetic testing helps reduce ADR risk by optimizing drug selection and dosage, particularly in monogenic disorders. Whole-exome sequencing of 6739 samples from the Russian population was performed on the DNBSEQ-G400 platform (MGI). Variants in 48 genes were examined, focusing on inherited arrhythmias, enzyme deficiencies (Glucose-6-Phosphate Dehydrogenase Deficiency [G6PDD], Porphyrias), Dravet Syndrome (DS) and Malignant Hyperthermia (MH). Variants reported as pathogenic (P), likely pathogenic (LP), or variants of uncertain significance (VUS) in ClinVar were manually re-evaluated using ACMG criteria. A total of 75 unique variants in 18 genes were observed in 119 individuals (1.77%), including 21 carriers and 13 women with a mutation. Of these, 44 variants were classified as P, 24 as LP, and 7 as VUS. Missense variants accounted for the largest proportion (73.33%). The most affected genes were (24/119), which exhibited the highest number of unique variants (18), (20/119), (15/119), and (14/119). Regarding associated conditions, mutations linked to arrhythmias were found in 51 individuals, MH in 27, G6PDD in 20, DS in 15, and Porphyrias in 6. Integrating common and rare clinically actionable genetic variants with attention to penetrance and clinical validity may improve medication safety, reduce preventable ADRs, and enhance personalized pharmacotherapy. - Source: PubMed
Publication date: 2026/05/28
Buianova Anastasiia ACheranev Valery VShmitko Anna OVasiliadis Iuliia ASamitova Alina FSuchalko Oleg NRepinskaia Zhanna AKuznetsov Mikhail IuBelova Vera AKorostin Dmitriy O - Chickpea (Cicer arietinum L.) is a nutritious food that contains bioactive peptides with hypoglycemic and antihyperglycemic activities. This study evaluated the antidiabetic effects of chickpea albumin hydrolysate (CAH) in rats with hyperglycemia induced by a high-fat diet (HFD) and streptozotocin (STZ). The CAH peptide profile was analyzed by liquid chromatography‒mass spectrometry. Five groups (n = 6) were established: one healthy control (HC) and four diabetic groups: diabetic control (DC), metformin (500 mg/kg body weight, b.w.; MET), CAH (200 mg/kg b.w.; H200), and CAH (400 mg/kg b.w.; H400). Food intake, body weight, and fasting blood glucose (FBG) were assessed weekly, and an oral sucrose tolerance test (OSTT) was performed. Blood and liver were analyzed for biochemical parameters (glucose and lipid profile), renal (urea and creatinine) and hepatic function (AST, ALT, and ALP), oxidative stress markers (GSH and MDA), gluconeogenic (PEPCK and G6Pase), and pentose phosphate (G6PD) enzymes, and PI3K/AKT and AMPK signaling pathways. CAH presented peptides predicted to inhibit DPPIV and α-glucosidase. OSTT showed that CAH (H200 and H400) reduced blood glucose levels by 18.6% and 22.8%, respectively, while metformin reduced them by 41.6%. CAH and metformin improved the lipid profile, decreased urea and creatinine levels, and attenuated elevations in hepatic enzymes. They showed antioxidant effects by increasing GSH and reducing MDA levels. CAH-treated rats showed pancreatic tissue restoration, reduced PEPCK and G6Pase activities, and increased G6PD activity. Exploratory immunoblotting analyses revealed qualitative differences in the phosphorylation of AMPK (muscle and liver) and AKT (muscle), which may be associated with the metabolic effects of CAH. These findings suggest that chickpea bioactive peptides could be helpful in the management of diabetes. - Source: PubMed
Navarro-Leyva AliciaLópez-Angulo GabrielaDelgado-Vargas FranciscoBastidas-Ponce AiméeSalazar-Salas Nancy YareliSoto-Lozoya Jenifer MarianaLópez-Valenzuela José Ángel - Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by dysregulated T cell responses and metabolic disturbances. Mesenchymal stromal cells (MSCs) have shown therapeutic promise, but their mechanisms, particularly concerning T cell metabolism, remain incompletely defined. This study investigated whether human umbilical cord-derived MSCs (hUC-MSCs) ameliorate collagen-induced arthritis (CIA) by modulating T cell metabolism and differentiation. - Source: PubMed
Wang XiaopingHe JingjingWang QunLiu XueYuan HaomingJin LuDing MengYang LinCui ShaoxinChang FeiXin TongJin HongtaoShi MinSong YongzhouPan WensenLiu Aijing