PBEF1 Blocking Peptide
- Known as:
- PBEF1 Blocking Peptide
- Catalog number:
- 33r-9851
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- PBEF1 Blocking Peptide
Related genes to: PBEF1 Blocking Peptide
- Gene:
- NAMPT NIH gene
- Name:
- nicotinamide phosphoribosyltransferase
- Previous symbol:
- PBEF1
- Synonyms:
- PBEF
- Chromosome:
- 7q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-02
- Date modifiied:
- 2014-11-19
Related products to: PBEF1 Blocking Peptide
Related articles to: PBEF1 Blocking Peptide
- Programmed axon degeneration (PAD; also known as Wallerian degeneration) is a conserved pathway controlling axon breakdown following injury or metabolic stress. PAD is driven by the depletion of nicotinamide adenine dinucleotide (NAD) through loss of the pro-survival enzyme NMNAT2 and activation of the pro-degenerative NADase SARM1. Recent genetic studies have identified pathogenic variants in PAD pathway enzymes associated with severe neurodegenerative phenotypes. - Source: PubMed
Publication date: 2026/06/24
Hopkins Eleanor LWilliams Pete A - Inhibition of the Src homology-2 domain containing protein tyrosine phosphatase-2 (SHP2) represents a promising therapeutic strategy for cancer. However, resistance to SHP2 inhibition, mediated by multiple mechanisms, has limited the clinical efficacy of SHP2 inhibitor monotherapy. Herein, we identified that nicotinamide phosphoribosyltransferase (NAMPT) inhibition could potentially overcome resistance to SHP2 inhibition in tumor cells. Compound was identified as the most potent dual inhibitor targeting SHP2 and NAMPT, exhibiting high inhibitory activity against both SHP2 and NAMPT. effectively inhibited proliferation in -insensitive tumor cell lines and reversed programmed cell death ligand 1 (PD-L1)-mediated immunosuppression. Furthermore, displayed significant antitumor efficacy in an MDA-MB-231 mouse model and strongly promoted antitumor immunity in a 4T1 mouse model. Our results identified as a promising dual SHP2 and NAMPT inhibitor, providing a novel therapeutic strategy for overcoming resistance to allosteric SHP2 inhibition. - Source: PubMed
Publication date: 2026/06/22
Wang KaizhenLiu YijiaoZhang ZhiyiHu YingxinZhong YuhuaJiang ShengZhang XiangyuZhang KuojunWang Tianyu - Chromosome 7 abnormalities -7 and -7q define a high-risk subset of myelodysplastic syndromes (MDS) with poor prognosis. The NAMPT gene, located at 7q22.3, encodes a rate limiting enzyme (nicotinamide phosphoribosyl transferase) in the NAD+ salvage pathway. Several inhibitors of NAMPT have been developed, but their activity in MDS has not been previously described. In this study, we investigated if MDS myeloblasts are susceptible to NAMPT inhibition. We show that primary bone marrow cells from patients with -7/-7q MDS exhibit strong and select sensitivity. Bulk viability assays and single cell, multiparametric flow cytometry confirmed enhanced NAMPT inhibitor sensitivity across leukemic cell populations, especially CD34 + CD38+ blasts from -7/-7q MDS samples compared to non -7/-7q MDS and healthy donor bone marrow cells. The NAMPT inhibitor KPT-9274 combined with BCL2 inhibitor venetoclax was particularly effective at targeting MDS blasts compared to NAMPT inhibition alone. MDS samples with -7/-7q also showed significantly lower NAMPT expression compared to the non -7/-7q samples, indicative of haploinsufficient gene expression profile. In conclusion, these findings support NAMPT haploinsufficiency as a vulnerability and as biomarker for NAMPT inhibitor activity in -7/-7q MDS. - Source: PubMed
Publication date: 2026/06/17
Ikonen NemoRuokoranta TanjaHyyppä SallaSinervuori EllaMiettinen Juho JSaad JosephVähä-Koskela MarkusHeckman Caroline A - The phase 3, randomized trial BRUIN CLL-321 assessed the safety and efficacy of pirtobrutinib versus investigators choice of idelalisib plus rituximab (IdelaR) or bendamustine plus rituximab (BR) in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) previously treated with a covalent BTK inhibitor. BRUIN CLL-321 showed significantly improved progression-free survival with pirtobrutinib compared to IdealR/BR. We report secondary endpoints including time to worsening (TTW) of CLL/SLL-related symptoms and physical function (PF). - Source: PubMed
Publication date: 2026/06/17
Ghia PaoloRossi DavideFerrant Emmanuellede la Cruz Vicente FátimaMaruyama DaiBanerji VershaCobb PatrickNamburi SwathiGreil RichardSharman Jeff PHess Lisa MPayakachat NalinBhandari Naleen RajRuppert Amy SWang DeniseAbada PaoloLoubert AngélyCreel KristinQiao CarolHan YimeiHill MarisaLeow Ching ChingCoombs Catherine CBarr Paul M - Disturbed mitochondrial activity in adipocytes has been proposed as one of the mechanisms involved in metabolic dysfunction in obesity. Glucagon-like peptide receptor agonists (GLP-1RAs) are used to normalize glucose level and reduce body weight. GLP-1 activates intracellular pathways similar to those of irisin, a peptide that modulates metabolism by stimulating the 'browning' of adipocytes. The aim of the study was to investigate the mechanisms of action of the GLP-1RA exendin-4 at the mRNA, protein, and mitochondrial levels in human adipocytes. - Source: PubMed
Publication date: 2026/04/03
Dziewońska AgnieszkaPolus AnnaGruca AnnaSolnica BogdanGóralska Joanna