Ask about this productRelated genes to: PDE4B antibody
- Gene:
- PDE4B NIH gene
- Name:
- phosphodiesterase 4B
- Previous symbol:
- DPDE4
- Synonyms:
- -
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-29
- Date modifiied:
- 2016-10-05
Related products to: PDE4B antibody
Related articles to: PDE4B antibody
- Phosphodiesterase 4 (PDE4) is a validated target for chronic inflammatory diseases such as COPD, asthma, and psoriasis. Although four PDE4 inhibitors have received FDA approval (roflumilast, apremilast, crisaborole, and ensifentrine), all suffer dose-limiting gastrointestinal side effects due to insufficient PDE4B/PDE4D selectivity. Plant-derived natural products offer complementary chemical space for discovering inhibitors with novel binding modes and improved isoform selectivity. This review systematically surveys plant-derived PDE4 inhibitors reported from 1979 to 2024, spanning seven major scaffold classes: flavonoids (∼40%), terpenoids, coumarins, xanthones, benzofurans, fluorenones, and alkaloids. Structure-activity analyses reveal that hydroxylation patterns, C2C3 unsaturation, and B-ring substitution govern flavonoid potency. Structure-guided optimization of toddacoumalone ultimately yielded compound 33a (IC = 3.1 nM, PDE4D), the fluorenone selaginpulvilin K (IC = 11 nM, 30-909-fold family selectivity), and a semi-synthetic α-mangostin derivative (IC = 17 nM). Despite promising potencies, critical gaps persist in subtype selectivity profiling, pharmacokinetic characterization, and metabolic stability. We propose that integrating AI-guided optimization, structure-informed isoform-selective design, nanodelivery systems, and biotechnology-enhanced production can accelerate clinical translation of these scaffolds. - Source: PubMed
Publication date: 2026/05/19
Huang Hao - This study aimed to identify genomic regions and candidate genes associated with body composition, and meat quality traits in Iberian pigs fattened in Montanera. A genome-wide association study (GWAS) was conducted on 528 pigs for 29 phenotypic traits using genomic data from the GGP Porcine HD Array. After quality control, 526 animals and 35,894 SNPs were retained for the association analysis. Despite the limitations of the genotyping chip used, which lacked coverage for Iberian-specific variants, the GWAS performed with GCTA software identified 165 SNPs significantly associated with 11 traits. Among these, 145 SNPs were clustered into 25 quantitative trait loci (QTL) regions. Five QTLs were identified for ham yield, containing genes such as KCNIP4, ZNF438, and PID1. Eight QTLs were associated with loin yield, with genes like PREX2, RSPO1, and PDE4B. One QTL was associated with shear force, and 16 QTLs were related to fatty acid composition. Genes linked to these traits included ELOVL6, associated with myristic and palmitic acids, and ADCY9 and ROBO1, associated with linoleic acid. Overall, these results provide novel genomic insights and markers that could enhance selection strategies in Iberian pig breeding programs, while highlighting the need for improved genomic tools tailored to local breeds. - Source: PubMed
Publication date: 2026/05/16
Palma-Granados PatriciaGarcía-Casco Juan MRamón ManuelDelgado-Gutiérrez Miguel ASánchez-Esquiliche FernandoMárquez AlbertoMuñoz María - Hypersensitivity pneumonitis (HP) is characterized by bronchiolocentric inflammation and fibrosis. The characteristic pathological features include bronchiolocentric inflammation, peribronchiolar fibrosis, and the presence of poorly formed granulomas. Nerandomilast is a novel oral phosphodiesterase 4 (PDE4) inhibitor with good selectivity for PDE4B. PDE4 inhibitors (PDE4i) exhibit anti-inflammatory/antifibrotic properties, the efficacy of nerandomilast remains unexplored in HP. - Source: PubMed
Publication date: 2026/05/14
Shi YujieLiu YumingLiu ZhigangChen RuxuanWang MengqiLi ZhiyiChen QiShao ChiLi XiaoheZhou HonggangHuang Hui - Nerandomilast, a selective phosphodiesterase 4B (PDE4B) inhibitor, has been extensively investigated for the treatment of pulmonary fibrosis; however, its therapeutic potential and mechanisms of action in idiopathic inflammatory myopathies-associated interstitial lung disease (IIM-ILD) remain to be elucidated. - Source: PubMed
Publication date: 2026/05/07
Cui XiLi WenjunChai HuiJiang YiGuo JinYang JumeiZhu JiaruiZhang Sigong - Idiopathic Pulmonary Fibrosis (IPF) is a progressive, fatal lung disease with a median survival of 3-5 years, driven by a profound unmet medical need. The current standard-of-care agents, pirfenidone and nintedanib, merely slow disease progression and are burdened by significant toxicity. This review synthesizes the basic, clinical, and translational evolution of novel pharmacological approaches for IPF, analyzing the critical lessons from recent high-profile clinical trial failures and successes. This review followed a narrative, analytical methodology, examining key Phase 2 and 3 clinical trials to identify a "failure-to-refinement" trajectory in drug development. Analysis reveals that targeting broad-spectrum enzymes (e.g., autotaxin via ziritaxestat) or downstream effectors (e.g., Connective Tissue Growth Factor (CTGF) via pamrevlumab) has failed, likely due to mechanistic redundancy or insufficient target engagement. In contrast, highly specific, next-generation inhibitors targeting upstream signal initiation points such as the lysophosphatidic acid receptor 1 (LPAR1) (admilparant) and local αv6 integrin-mediated activation of transforming growth factor-beta (TGF-β) (bexotegrast) have yielded promising Phase 2 data, demonstrating a sophisticated translational learning loop. Furthermore, the geroscience approach targeting cellular senescence (dasatinib/quercetin) has introduced a controversial new paradigm, while the recent approval of nerandomilast (a phosphodiesterase 4B (PDE4B) inhibitor) establishes a new therapeutic class. The IPF pipeline has matured, moving from broad attenuation toward specific, mechanism-based inhibition. This shift, informed by interpreting trial failures, is guiding the development of therapies toward disease modification and combination strategies, offering a tangible path toward curative-intent treatments. - Source: PubMed
Publication date: 2026/04/21
Mansour Ghaith KHajjar Ahmad WSukkarieh Hatouf H