Drug Database
FA

famotidine (Pepcid RPD / Pepcidin Rapitab / famotidine, Zydis)

✓ Approved

Merck & Co. · HRH2 · Small Molecule

What is famotidine?

famotidine is a small molecule developed by Merck & Co.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesPepcid RPD, Pepcidin Rapitab, famotidine, Zydis
CompanyMerck & Co.
Drug ClassSmall Molecule
Molecular TargetHRH2
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Merck & Co.

Mechanism of Action

Molecular Targets

famotidine acts on 1 molecular target:

HRH2histamine receptor H2 (H2R, HH2R)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

famotidine is developed for 3 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Gastrointestinal disordersDuodenal ulcer✓ Approved
Gastrointestinal disordersGastric ulcer✓ Approved
Gastrointestinal disordersGastrooesophageal reflux disease✓ Approved

Related Research Articles

PubMedEuropean journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V2026-09-16

Conformational flexibility governs phosphate-induced solubility enhancement: a comparative study of cimetidine and famotidine by pH-dependent dissolution, NMR titration, DOSY, and DFT analysis.

Tsunoda Chihiro C, Goto Satoru S, Hiroshige Ryosuke R, Hasegawa Kanji K et al.

Inorganic phosphate buffers are widely used in pharmaceutical dissolution testing, yet the direction of their effect on drug solubility is not uniform across solutes: for some basic drugs, phosphate decreases apparent solubility through insoluble salt formation or ionic-strength effects, while for others, our prior work has documented concentration-dependent solubility changes inconsistent with either mechanism. We report here that phosphate selectively increases the apparent cationic solubility of cimetidine (CIM) up to 2.6-fold but has a negligible effect on famotidine (FAM), two structurally distinct H2-receptor antagonists, across a range of pH values and buffer compositions. This solubility-enhancing effect is mechanistically distinct from the well-documented solubility-decreasing effects of phosphate reported for other basic drugs via insoluble salt formation or ionic-strength suppression; those mechanisms predict a concentration-dependent decrease in solubility, which is thermodynamically incompatible with the concentration-dependent increase observed here for CIM. The differential response between CIM and FAM cannot be explained by classical Henderson-Hasselbalch ionization models or by differences in pH or buffering capacity. Three independent experimental approaches converge on a consistent interpretation. pH-dependent solubility measurements showed that phosphate selectively increases the cationic solubility (Si) of CIM while leaving the neutral-form solubility (S0) unchanged; FAM showed no significant Si response. 1H NMR titration revealed progressive downfield shifts of CIM imidazole resonances (∼1.0 ppm over 10-100 mM phosphate) with vicinal coupling constants consistent with a shift toward the cis/gauche (Zusammen) conformation; FAM and histamine responded minimally (∼0.5-0.6 ppm). DOSY diffusion measurements showed that phosphate decreases CIM diffusion disproportionately relative to bulk viscosity, indicating stronger solute-solvent coupling for the conformationally flexible molecule. DFT-based Boltzmann analysis reveals that CIM possesses a broad low-energy conformer ensemble (partition function Z = 2.62), whereas FAM is dominated by a single rigid geometry (Z = 1.10). The correlation between conformational entropy and phosphate-induced solubility enhancement suggests that molecular flexibility is a key determinant of ion-specific buffer effects, with implications for BCS solubility classification using phosphate-buffered media.

PMID 42749025
Read full article →
PubMedAnalytical and bioanalytical chemistry2026-09-15

Efficient determination of ranitidine, famotidine, and cimetidine in environmental and biological matrices using a NH₂-bimetallic MIL-88(Fe/Ni)@SiO₂/Fe₃O₄ composite and dispersive micro solid-phase extraction.

Motamedifar Fahimeh F, Masrournia Mahboubeh M, Khoshnood Razieh Sanavi RS

The widespread use of gastrointestinal drugs like ranitidine, famotidine, and cimetidine has led to their emergence as persistent environmental contaminants, while their monitoring in biological fluids remains crucial for clinical toxicology. This study presents the development of a sensitive and efficient analytical method based on dispersive micro solid-phase extraction (d-μ-SPE) coupled with high-performance liquid chromatography-photodiode array detector (HPLC-DAD) for their determination. A novel magnetic adsorbent, NH₂-bimetallic MIL-88(Fe/Ni)@SiO₂/Fe₃O₄, was synthesized and characterized. The unique bimetallic system and amine functionalization of the metal-organic framework (MOF) provided specific interactions with the target analytes, while the silica shell ensured stability, and the magnetic core facilitated separation. The critical factors affecting the d-μ-SPE efficiency were optimized using a two-stage experimental design: a definitive screening design (DSD) identified pH, sorbent dose, desorption time, and solvent volume as significant, and a subsequent central composite design (CCD) modeled their quadratic effects. Under optimal conditions, the method demonstrated low limits of detection (0.02-0.07 ng mL⁻1), high enrichment factors (59.3-72.5), and good precision (RSD < 5%). The method was successfully applied to tap, river, and well water, as well as human urine samples, achieving excellent relative recovery rates (89.8-95.3%), even in samples from individuals who had ingested the drugs. The adsorbent could be reused for three cycles without significant loss in performance.

PMID 42742695
Read full article →
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
Read full article →
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
Read full article →
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
Read full article →
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
Read full article →

+2400 more articles available with a free account

Sign up free to view all articles →

Ask about famotidine