Ask about this productRelated genes to: PDE4B Blocking Peptide
- 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 Blocking Peptide
Related articles to: PDE4B Blocking Peptide
- Oral lichen planus (OLP) is a chronic inflammatory mucosal disease with a risk of malignant transformation and limited long-term therapeutic options. Paeoniflorin (PF), a natural monoterpene glycoside, exhibits multi-target anti-inflammatory and immunomodulatory properties, but its systematic mechanisms against OLP remain elusive. - Source: PubMed
Publication date: 2026/07/17
Zhao TianChen QiYu Liang - Alzheimer's disease (AD) is a complex neurodegenerative condition marked by a gradual loss of cognitive function, impaired synaptic signalling, and sustained neuroinflammatory responses. Among the molecular pathways associated with disease progression, cyclic adenosine monophosphate (cAMP) signalling, plays a crucial factor in disruption of cellular homeostasis. Phosphodiesterase-4 (PDE4), especially the PDE4B isoform, controls intracellular cAMP levels in neuronal and glial cells, which affects inflammatory signalling and synaptic plasticity in the brain. Therefore, selectively targeting PDE4B is a novel approach to identify the small molecule's therapeutic activity to restore the cAMP signalling, with parallel regulation of the dose-limiting side effects. GSK356278 and Rolipram are the known PDE4B modulators, which have been considered for the current study to generate significant pharmacophoric features and execute drug design as CNS-active PDE4B inhibitors. Six heterocyclic derivatives were designed and synthesised by altering the core scaffold in order to maximise hydrophobicity, CNS permeability, and Q-pocket engagement without depending on direct Zn or Mg coordination. Among these, molecule VCHH-19 and VCPH-19 demonstrated significant CNS compatibility and good binding stability. PC12 cell lines were chosen to verify the neuroprotective response, and the Drosophila model for for AD assessment. All of these results indicated the significance of pyridine-based heterocycles molecules as potential candidates for PDE4B-targeted AD treatment. - Source: PubMed
Publication date: 2026/07/23
Pujar Karthik GPurohit DipenShetty Richa PrabhakarS ParthasarathiKolachi Krishna YallappaBharathi H M AishwaryaAchar Pooja GandharvachariP Prabitha - To review the emerging evidence supporting the use of nerandomilast (Jascayd), a selective phosphodiesterase-4B (PDE4B) inhibitor, for the treatment of idiopathic pulmonary fibrosis (IPF) and progressive pulmonary fibrosis (PPF). The review aims to summarize its mechanism of action, efficacy, safety, and potential role as monotherapy or in combination with existing antifibrotic therapies. A literature search was conducted using PubMed, Embase, ClinicalTrials.gov, and relevant conference proceedings from January 2018 through December 2025. Search terms included , , , , , , , , and . Human studies published in English were included. Original clinical studies, phase II and phase III trials, subgroup analyses, and regulatory publications evaluating nerandomilast in patients with IPF or PPF were reviewed. Studies were selected based on relevance to efficacy, safety, mechanism of action, and clinical outcomes. Data regarding study design, patient population, forced vital capacity (FVC) outcomes, adverse events, and concomitant antifibrotic use were extracted and qualitatively synthesized. Nerandomilast was approved in October 2025 for the treatment of IPF and PPF, representing the first PDE4B inhibitor approved for fibrotic lung disease. By inhibiting PDE4B, nerandomilast increases intracellular cyclic adenosine monophosphate (cAMP) levels, resulting in reduced inflammatory cytokine production and decreased fibroblast activation. Clinical trials, including the phase III FIBRONEER-IPF study, demonstrated a significant reduction in the rate of FVC decline compared with placebo, indicating attenuation of disease progression. Benefits were observed both in patients receiving nerandomilast alone and in those receiving background antifibrotic therapy with pirfenidone or nintedanib. Overall, nerandomilast demonstrated a favorable benefit-risk profile and offers a mechanistically distinct approach compared with currently available antifibrotic agents. Nerandomilast provides a novel anti-inflammatory and antifibrotic treatment option for patients with IPF and PPF. Available evidence suggests meaningful reductions in lung function decline with acceptable tolerability, including use alongside established antifibrotic therapies. As longer-term and real-world data emerge, nerandomilast may become an important component of the therapeutic strategy for progressive fibrotic lung diseases. - Source: PubMed
Publication date: 2026/07/16
Bishop KellySantana Janeliz MercadoDietrich EricVascimini Angelina - Preferential phosphodiesterase 4B (PDE4B) inhibition with nerandomilast has demonstrated attenuation of forced vital capacity decline in idiopathic pulmonary fibrosis and progressive pulmonary fibrosis. Because PDE4 enzymes regulate cAMP-dependent inflammatory and endothelial signalling, class-level PDE4 inhibition has been consistently linked to vascular-immune pathways. Whether preferential PDE4B inhibition reproduces these effects remains uncertain. - Source: PubMed
Publication date: 2026/07/22
Perrotta FabioMariniello Domenica FrancescaPagliaro RaffaellaBianco Andrea - Problematic alcohol use (PAU) and anxiety disorders (ANX) frequently co-occur, implying shared genetic and neurobiological foundations. However, the directionality of potential causal relationships and the specific mechanisms underlying the overlap remain unclear. Thus, we investigated the shared genetic architecture and neurobiological pathways between PAU and ANX using a multimethod genomic approach. We analyzed summary statistics from genome-wide association studies (GWAS) of PAU and ANX using Mendelian Randomization to assess causal associations between ANX and PAU. We used MiXeR to assess the overall shared genomic architecture, Local Analysis of (co)Variant Association to estimate regional genetic correlations, and conjunctional false discovery rate (conjFDR) to identify individual overlapping loci. We used FUMA to map single-nucleotide polymorphisms (SNPs) to independent loci, conduct differential gene expression analyses across 30 general and 54 specific tissue types, and perform cell-type specificity analyses using a human brain cell atlas. Druggability of identified targets was also evaluated. Mendelian Randomization analyses indicated bidirectional causal associations between ANX and PAU. MiXeR identified moderate polygenic overlap (52.5%) and genetic correlation (r = 0.44) between the traits, with high effect direction concordance among shared estimated causal variants (86.4%). ConjFDR identified 97 shared lead SNPs, of which 89 had concordant and 8 discordant effects on PAU and ANX. These loci mapped to 97 genes, including DRD2 and PDE4B, genes linked to dopaminergic and cAMP signaling pathways, respectively. Concordant gene expression was enriched in brain, nerve, adrenal gland, esophagus, stomach, and colon, with enriched expression specifically in the prefrontal cortex, anterior cingulate cortex, hippocampus, hypothalamus, substantia nigra and amygdala. FUMA cell-type enrichment analysis identified associations predominantly in neurons from the cerebral cortex, hippocampus, and thalamus. We found substantial genetic and neurobiological overlap between PAU and ANX, highlighting reciprocal, causal relationships between the traits, with differentially expressed genes enriched in addiction- and anxiety-relevant brain regions. These findings support shared genetic and neurobiological mechanisms linking PAU and ANX, while acknowledging that some signals may reflect broader internalizing or psychiatric liability. - Source: PubMed
Publication date: 2026/07/13
Shi MingjianGunawan TommyMalone Samantha GSetzer MichaelPiserchia ZacharyDavis Christal NRentsch Christopher TFriligkou EleniZhou HangPolimanti RenatoWang LuVaitinadin Nataraja SarmaKranzler Henry RGray Joshua C