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famotidine (Gaster D / Gaster OD / famotidine, WOWTAB)

✓ Approved

Astellas Pharma · HRH2 · 小分子

什么是 famotidine？

famotidine 是一种小分子，由Astellas Pharma研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Gaster D, Gaster OD, famotidine, WOWTAB
公司Astellas Pharma
药物类别小分子
分子靶点HRH2
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Astellas Pharma

作用机制

分子靶点

famotidine 作用于 1 个分子靶点：

HRH2histamine receptor H2 (H2R, HH2R)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

famotidine 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Gastrointestinal disordersGastric ulcer✓ Approved
Gastrointestinal disordersGastritis✓ Approved

相关研究文献

PubMedCrystal growth & design2026-09-10

Enhanced Solubility of Famotidine through Salification.

Eilers Jane M JM, Seo Payton P, Ma Liulei L, Kelley Steven P SP et al.

Famotidine (FMT) is an active pharmaceutical ingredient that exhibits poor aqueous solubility and poor permeability. Molecular electrostatic potential and pK a calculations were used to guide a salification strategy for FMT and afforded five salts featuring carboxylic acid-containing coformers. All solids feature charge-assisted hydrogen bonds between the guanidinium group of FMT and carboxylate of the coformer. All salts exhibited good thermal and benchtop stability, and a six- to 20-fold increase in aqueous solubility was achieved, depending on the coformer used. The best performing salts include coformers on the FDA's generally recognized as safe list, making the solids promising for pharmaceutical applications.

PMID 42719395
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PubMedEBioMedicine2026-09-04

Discovering repurposable drugs for Alzheimer's disease and related dementias: target trial emulation using decentralised real-world data.

Wu Qiong Q, Li Lu L, Lei Yuqing Y, Zhou Ting T et al.

Alzheimer's disease and related dementias (ADRD) affect nearly 6.9 million Americans, with the number expected to triple by 2050, while disease-modifying therapies remain unavailable. Drug repurposing, which identifies new indications for already approved medications, offers a more efficient and cost-effective pathway to accelerate development of effective therapies for ADRD. The aim of this study is to identify potential drug repurposing signals by systematically screening routinely prescribed drugs for associations with progression from mild cognitive impairment (MCI) to ADRD. We conducted a multi-site target trial emulation using electronic health record (EHR) data from four decentralised databases: INSIGHT Clinical Research Network, OneFlorida + Clinical Research Consortium, the University of Pennsylvania Health System, and Yale New Haven Health System. We performed an independent validation using EHR data from the TriNetX Research Network and a genetic risk-stratified sensitivity analysis in the Penn Medicine BioBank (PMBB) database. Eligible participants were adults aged 50 years or older at the time of MCI diagnosis, with no prior diagnosis of ADRD and no prior use of the trial drugs. Initiation of each of 181 routinely prescribed drugs was compared with two active control groups defined by initiation of supplements or cardiovascular medications. Risk ratios (RRs) and 95% CIs were estimated using a federated target trial emulation framework (LATTE) with stabilised inverse probability of treatment weighting and Poisson regression. A total of 122,972 eligible patients were identified from the four decentralised databases, 335,506 patients identified from the TriNetX network for validation and 898 from PMBB database. Federated, multi-site target trial emulation identified 20 drug repurposing hypotheses with statistically significant protective effects, including anti-inflammatory and pain-modulating agents (celecoxib: RR 0.43; 95% CI: 0.23-0.81; dexamethasone RR 0.46; 95% CI: 0.29-0.73; gabapentin: RR 0.55; 95% CI: 0.36-0.83; ketorolac: RR 0.50; 95% CI: 0.31-0.80; methylprednisolone: RR 0.43; 95% CI: 0.24-0.76; prednisone: RR 0.48; 95% CI: 0.28-0.83; pregabalin: RR 0.53; 95% CI: 0.35-0.79), antimicrobial and microbiome-associated agents (cefazolin: RR 0.62; 95% CI: 0.45-0.84; clavulanate: RR 0.56; 95% CI: 0.44-0.71; fluconazole: RR 0.36; 95% CI: 0.23-0.58), neuromodulators and adrenergic agents (epinephrine: RR 0.42; 95% CI: 0.31-0.56; propranolol: RR 0.56; 95% CI: 0.37-0.85; salmeterol: RR 0.49; 95% CI: 0.32-0.74; tizanidine: RR 0.29; 95% CI: 0.14-0.57), vascular, metabolic, and hormonal modulators (empagliflozin: RR 0.29; 95% CI: 0.17-0.50; oestradiol: RR 0.47; 95% CI: 0.28-0.81; ezetimibe: RR 0.69; 95% CI: 0.52-0.91; sodium bicarbonate: RR 0.49; 95% CI: 0.29-0.84; spironolactone: RR 0.43; 95% CI: 0.31-0.60), and histamine-related and gastrointestinal agents (famotidine: RR 0.64; 95% CI: 0.55-0.74). Results were consistent in the independent validation using TriNetX network and sensitivity analysis in PMBB database. 20 widely used medications may be associated with reduced progression from MCI to ADRD and represent promising candidates for clinical evaluation as repurposed therapies for dementia. National Institutes of Health.

PMID 42697072
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PubMedInflammopharmacology2026-08-26

Empagliflozin protects against indomethacin-induced gastric injury in rats: evidence from inflammatory, apoptotic, and early PI3K/Akt/VEGF-related changes.

Toprak-Semiz Ayça A, Topçu Atilla A, Deniz Esra E, Öztürk Çiğdem Ç et al.

Non-steroidal anti-inflammatory drugs (NSAIDs), particularly indomethacin, are widely used for the treatment of pain and inflammation but frequently cause gastric mucosal injury. Empagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor primarily used for type 2 diabetes, has recently attracted attention due to its anti-inflammatory, antioxidant, and cytoprotective properties. The present study investigated the potential gastroprotective effects of empagliflozin against indomethacin-induced gastric injury in rats and explored the underlying mechanisms related to inflammation, oxidative stress, apoptosis, and PI3K/Akt/VEGF-related signaling pathways. Male Sprague-Dawley rats were divided into six groups: control, indomethacin, indomethacin + famotidine, indomethacin + empagliflozin (10 mg/kg), indomethacin + empagliflozin (20 mg/kg), and empagliflozin (20 mg/kg). Rats were pretreated with empagliflozin for 7 days before induction of acute gastric injury with indomethacin. Gastric tissues were evaluated using biochemical, histopathological, immunohistochemical, and Western blot analyses. Indomethacin administration significantly increased pro-inflammatory cytokines (TNF-α and IL-6), reduced prostaglandin E2 levels, and increased cleaved caspase-3 expression, indicating activation of inflammatory and apoptotic pathways. Empagliflozin treatment significantly reduced inflammatory cytokine levels, restored prostaglandin levels, and suppressed cleaved caspase-3 expression, while oxidative stress-related parameters showed limited and non-uniform changes. In addition, empagliflozin was associated with changes in cyclooxygenase activity and PI3K/Akt/VEGF-related signaling in this acute injury model. Histopathological findings were generally consistent with the biochemical results and suggested partial improvement in gastric mucosal damage following empagliflozin treatment. Taken together, these findings indicate that empagliflozin exerts gastroprotective effects mainly through modulation of inflammatory and apoptotic pathways, with accompanying early changes in oxidative stress-related parameters and PI3K/Akt/VEGF-related signaling. These results suggest that empagliflozin may represent a potential candidate for the prevention of NSAID-induced gastric injury.

PMID 42645721
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PubMedFood science & nutrition2026-08-04

Gastroprotective Effects of Nettle- and Carob-Enriched Snail Mucus in a Rat Model of Gastric Injury: Role of Antioxidant and Anti-Inflammatory Mechanisms.

Gharbi Khaoula K, Selmi Slimen S, Wahabi Soumaya S, Kahlaoui Hanen H et al.

Dietary supplementation of Helix aspersa Müller with nettle (Urtica dioica L.) or carob (Ceratonia siliqua L.) has been hypothesized to enhance the biochemical composition and gastroprotective properties of the secreted mucus through enrichment of its polyphenolic, protein, and glycoprotein content. This study presents a comprehensive experimental evaluation of diet-enriched snail mucus preparations across three supplementation levels (10%, 20%, and 30%) in an ethanol-induced rat gastric ulcer model, encompassing phytochemical characterization, in vitro antioxidant assessment, and in vivo biochemical, systemic, and histopathological profiling. A standard snail mucus control group (SSSD) was included to isolate the specific contribution of dietary plant enrichment from the intrinsic properties of snail mucus itself. Analysis revealed that dietary supplementation significantly increased the yield of lyophilised snail mucus as well as its total phenolic, flavonoid, protein, and sugar contents in a dose-dependent manner, with nettle exerting markedly superior effects than carob at all tested doses, attributable to its 33-fold higher phenolic content and 15.5-fold higher flavonoid content relative to carob extract. In vivo, pretreatment with enriched mucus preparations significantly attenuated ethanol-induced gastric injury across all evaluated parameters. The 30% nettle-enriched group (SSUD30%) demonstrated the strongest gastroprotective effect, normalizing gastric pH (3.75 ± 0.074), reducing gastric juice volume (1.59 ± 0.071 mL/100 g), restoring antioxidant enzyme activities (SOD, CAT, GPx) to near-control values, reducing lipid peroxidation markers (MDA: 0.35 nmol/mg protein), and attenuating systemic inflammatory biomarkers including CRP, hepatic enzymes, and lipid profile alterations. Histopathological semi-quantitative scoring confirmed a histological damage score reduction from 11 (ethanol group) to 2 in the SSUD30% group, corresponding to 81.82% protection, significantly exceeding that of famotidine (36.3%). These findings support a comprehensive gastroprotective model based on three complementary and interdependent mechanisms: reinforcement of the physical mucus barrier through increased viscosity and glycoprotein content, enhancement of endogenous antioxidant defenses through restoration of SOD, CAT, and GPx activities via the Nrf2/HO-1 pathway, and attenuation of systemic inflammatory cascades through inhibition of NF-κB-mediated signaling by flavonoids and polyphenols incorporated into the enriched mucus. Overall, diet-enriched snail mucus, particularly SSUD30%, should be conceptualized not merely as a topical mucoprotective agent, but as a multi-target bioactive preparation whose efficacy depends on the complementary contribution of physical barrier reinforcement, antioxidant restoration, and anti-inflammatory modulation. Future studies should prioritize identification of the specific bioactive compounds responsible for the observed effects, assessment of bioavailability under gastrointestinal conditions, and validation of therapeutic potential in human clinical settings.

PMID 42549096
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PubMedThe Lancet. Infectious diseases2026-07-09

Efficacy and safety of rivaroxaban, colchicine, and famotidine-loratadine with specialist supportive clinical care for fatigue in patients with post-COVID-19 condition in the UK: a multisite, open-label, randomised controlled trial.

STIMULATE-ICP consortium

Post-acute sequelae of COVID-19 or post-COVID-19 condition (also known as long COVID) affects 1-5% of adults globally, most commonly with fatigue, and no evidence-based therapies are available. We aimed to evaluate the efficacy of repurposed medications in fatigue management in adults with long COVID. We did a phase 3, four-group, randomised, controlled, adaptive platform, open-label drug trial nested within a pragmatic, multicentre, cluster-randomised trial of an integrated care pathway (ICP) for long COVID across 12 UK National Health Service (NHS) specialist long COVID care clinics in the UK. Participants had to be adults (>18 years) with long COVID who had not been hospitalised with COVID-19. In addition to NHS specialist-led long COVID care (hereafter, usual care), participants in the ICP trial could receive multiorgan MRI and clinical decision support and/or app-based rehabilitation. Initially, participants in the ICP trial were invited to enrol in the drug trial, but slow recruitment to the drug trial led to establishment of additional drug-only trial sites. Participants enrolled at either ICP trial sites or drug-only trial sites were randomly assigned (1:1:1:1) to receive colchicine 500 μg twice daily, rivaroxaban 10 mg once daily, famotidine 40 mg with loratadine 10 mg once daily, or no drug for 12 weeks. All participants received usual care. Randomisation was done electronically in blocks (various block sizes) and stratified by site, birth sex, ICP trial group allocation, and being a new or previous patient of a drug-only site. The primary endpoint was 12-week fatigue, assessed with the Fatigue Assessment Scale (FAS; with scores ranging from 10 [no fatigue] to 50 [debilitating fatigue], and a >10% change considered clinically meaningful) among randomly assigned individuals who had available baseline and 12-week data, adjusting for baseline fatigue and clinically relevant covariates. Secondary endpoints included 24-week FAS. The nested drug trial is registered, ISRCTN10665760. The trial is complete. Of 6035 eligible participants, 778 (383 co-enrolled in the ICP trial and 395 directly enrolled in the drug trial) were randomly assigned between Aug 22, 2022, and Aug 7, 2024 to colchicine (n=192), famotidine-loratadine (n=193), rivaroxaban (n=197), or no drug (usual long COVID care only; n=196). The mean age of participants was 46 years (SD 12·4), 495 (64%) of 778 were female, and 91 (12%) were from a non-White ethnic group. Across all trial groups, there was severe baseline fatigue (mean FAS score 36·8 [SD 7·49]) and a clinically relevant mean FAS reduction of 4·3 points to 32·5 (SD 9·13) at 12 weeks. Adjusted analyses showed small, statistically significant FAS reductions in the colchicine (-1·49 points [95% CI -2·92 to -0·06], p=0·041) and famotidine-loratadine (-1·48 points [-2·88 to -0·08], p=0·038) groups, but not in the rivaroxaban group (-1·06 points [-2·47 to 0·35, p=0·139), compared with no study drug at 12 weeks. However, 24-week FAS scores, 12 weeks after drug cessation, were not significantly different between groups. Treatment was well tolerated, with ten serious adverse events (requiring hospitalisation but unrelated to trial drugs) reported in eight (1·0%) of the 778 participants, five of which were in three participants in the rivaroxaban group. In participants with long COVID, severe fatigue reduced in all study groups-including the no drug group-over 12 weeks, with small additional reductions in the colchicine and famotidine-loratadine groups compared with the no drug group. Modest effects on FAS were not sustained after drug withdrawal. Long-term long COVID symptom benefit is unlikely with these drugs alone. Future trials could investigate the use of these or other repurposed drugs in specific subgroups of patients with long COVID, combination therapies, and how care is delivered. UK National Institute for Health and Care Research.

PMID 42419335
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PubMedMolecular biology reports2026-07-08

BDNF and GSK-3β signaling in depression: molecular mechanisms underlying neural plasticity dysfunction.

Al-Kuraishy Hayder M HM, Abass Shimaa A SA, Mahana Hitham Alaa Mohammed HAM, Elbanna Osama Ashraf OA et al.

Depression, a complicated psychiatric condition, is characterized by persistent low mood, disrupted emotional regulation, and cognitive impairment. Attenuated brain-derived neurotrophic factor (BDNF) and dysregulated glycogen synthase kinase-3 beta (GSK-3β) activity promote synaptic deterioration, oxidative imbalance, neuroinflammatory responses, and hippocampal dysfunction, hallmark features of depressive pathology. This review provides an overview of current preclinical and clinical findings explaining the independent and interactive roles of BDNF and GSK-3β in depression. It further illustrates emerging therapeutic approaches targeting this axis, such as metformin, famotidine, tideglusib, lithium, and ketamine. Collectively, the altered crosstalk between BDNF and GSK-3β contributes to the impaired neuroplasticity observed in depression, suggesting that this signaling axis is a promising therapeutic target.

PMID 42417900
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