Drug Database
IB

ibuprofen (ibuprofen, Scherer)

✓ Approved

Cardinal Health, Inc. · PTGS1 · Small Molecule

What is ibuprofen?

ibuprofen is a small molecule developed by Cardinal Health, Inc.. It is approved for therapeutic indications via topical.

Drug Profile

Brand Namesibuprofen, Scherer
CompanyCardinal Health, Inc.
Drug ClassSmall Molecule
Molecular TargetPTGS1, PTGS2
RouteTopical
StatusApproved
Sources: ClinicalTrials.gov, Cardinal Health, Inc.

Mechanism of Action

Molecular Targets

ibuprofen acts on 2 molecular targets:

PTGS1prostaglandin-endoperoxide synthase 1 (COX3, PCOX1)
PTGS2prostaglandin-endoperoxide synthase 2 (GRIPGHS, hCox-2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

ibuprofen is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Gastrointestinal disordersAbdominal pain✓ Approved
Musculoskeletal and connective tissue disordersMusculoskeletal pain✓ Approved
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved

Related Research Articles

PubMedJAMA network open2026-11-10

Ibuprofen Use and Acute Kidney Injury Among Adults Admitted to the Hospital.

Thelen Haedi E HE, Keele Luke J LJ, Brotman Christina C, Shashaty Michael G S MGS et al.

Although nonsteroidal anti-inflammatory drugs (NSAIDs) are the most effective nonopioid analgesics for acute pain, they may be underused in the inpatient setting due to uncertainty regarding the risk of acute kidney injury (AKI). Whether inpatient exposure to NSAIDs, such as ibuprofen, substantially increases AKI risk and how ibuprofen-associated AKI varies across patient subgroups remain unknown. To determine whether ibuprofen use is associated with AKI in hospitalized patients and whether the finding varies across AKI risk factor subgroups. A retrospective active-comparator cohort study of hospitalized patients (aged ≥18 years) without end-stage kidney disease or contraindications to NSAID treatment admitted from January 1, 2004, to June 30, 2017, in a large academic health system including 3 hospitals in Philadelphia, Pennsylvania, with follow-up until 48 hours after treatment end, hospital discharge, or 14 days elapsed, whichever occurred first. Analyses were conducted from March 2023 through August 2026. At least 24 hours of treatment with ibuprofen or oxycodone for acute pain. The primary outcome was AKI, defined by changes in serum creatinine and incident kidney replacement therapy (KRT). Balancing weights were used to adjust for baseline covariates and weighted Poisson regression used to estimate incidence rate ratios (IRRs) and 95% CIs. This study included 78 656 patients (median age, 59 [IQR, 47-69] years; 38 092 females [48%]) treated with ibuprofen (n = 6313) or oxycodone (n = 72 343). There were 4799 AKI events (79% stage 1) during 270 472 days of follow-up (17.7 events per 1000 days). After adjustment for baseline differences, patients treated with ibuprofen had a higher rate of any AKI (IRR, 1.22; 95% CI, 1.09-1.38), severe AKI (IRR, 1.36; 95% CI, 1.08-1.72), and KRT (IRR, 3.29; 95% CI, 1.35-8.03). IRRs were greater in postoperative (IRR, 1.70 [95% CI, 1.28-2.27] vs 1.12 [95% CI, 0.98-1.28]) and critically ill (IRR, 1.65 [95% CI, 1.29-2.11] vs 1.16 [95% CI, 1.02-1.33]) patients. In patients at low risk (those non-critically ill, nonpostoperative, aged <60 years without kidney dysfunction; ibuprofen, n = 2966; oxycodone, n = 20 440), ibuprofen was not associated with higher AKI risk (IRR, 0.94; 95% CI, 0.75-1.18). This study in an inpatient cohort found that ibuprofen was associated with higher rates of AKI and KRT, but this excess risk was concentrated in patients at high risk. Patients at low risk may be able to receive ibuprofen safely yet were often prescribed oxycodone.

PMID 43007674
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PubMedPediatric nephrology (Berlin, Germany)2026-11-10

Patent ductus arteriosus and neonatal acute kidney injury-a comparative analysis of treatment strategies.

Wildes Dermot D, Kuhar Maja M, Mullaly Rachel R, Riordan Michael M et al.

To evaluate the impact of ductal treatment timing, treatment modality and cumulative ductal exposure on the incidence of acute kidney injury (AKI) in very preterm infants with patent ductus arteriosus (PDA). Additionally, to determine whether high-risk PDA phenotype is independently associated with AKI after adjustment for confounding variables, and to assess whether the initial medical agent for ductal closure is associated with post-treatment AKI. We conducted a retrospective study of 184 infants born under 29 weeks' gestation admitted to a tertiary neonatal unit between 2020-2023. PDA severity was stratified using the El-Khuffash PDA score (high risk ≥5). AKI was defined using the modified neonatal KDIGO criteria. Time-anchored outcomes were used to address AKI temporality. Multivariable bias-reduced logistic regression was performed to control for gestational age, condition at birth, gender and small-for-gestational-age status. Median gestational age was 26.6 weeks with a median birth weight of 863 g. AKI occurred in 28/175 infants (16%) with 20/28 (71%) occurring by day of life fourteen. AKI incidence was 19.6% in the high-risk, refractory to medical treatment infants, 21.8% in the high-risk responsive to medical treatment infants and 8.7% in low-risk infants. Among high-risk treated infants, post-treatment AKI occurred in 17.1% with no discrepancy between paracetamol-first (14.7%) and ibuprofen-first (18.3%) strategies (adjusted OR 1.63, 0.49-5.48). In this cohort of premature infants with PDA, AKI was common in crude analyses. Among high-risk treated infants, ibuprofen-first treatment strategy was not associated with increased post-treatment AKI, though estimates were imprecise and confounding by indication remains likely.

PMID 43007428
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PubMedInternational journal of pharmaceutics2026-11-10

Dissolution coning in USP apparatus II - Part I: quantifying formulation-dependent coning severity with the drug entrapment fraction (DEF).

Bhat Roopal R, Kossor Christopher C, Tripathi Siddharth S, Bao Quanying Q et al.

Dissolution coning is the accumulation of disintegrated particles beneath the paddle in USP Apparatus II that can confound dissolution interpretation due to drug retention within the deposit. Visual qualitative observations or hydrodynamic suspension criteria, such as no-coning rpm (NCrpm), do not measure the impact of coning on drug release. Hence, coning behavior across different tablet formulations is examined in Part I with an intent to propose a quantitative metric to classify its severity. Immediate-release ibuprofen (BCS Class II) tablets formulated with microcrystalline cellulose (MCC; Avicel pH 102) or three grades of dibasic calcium phosphate anhydrous (Fujicalin, A-Tab, Calipharm A) at drug loadings (DL) of 20, 50, and 70% w/w were considered. Distinct dissolution responses were observed, ranging from complete release despite cones for MCC to substantial drug entrapment (Fujicalin < A-Tab < Calipharm A), even with comparable or lower NCrpm. Coning severity could not be explained by particle size or terminal settling velocity. Consequently, the extent of incomplete dissolution characterized as drug entrapment fraction (DEF) was used for the first time as a quantitative metric to quantify coning severity. DEF enabled linking cone formation with dissolution performance, providing a formulation-relevant measure of coning severity. It exhibited distinct trends among the excipient systems and increased as the drug: filler ratio decreased. This trend was qualitatively consistent with visible cone and surrounding zone structure where higher-DEF formulations exhibited more compact clearly defined cones. Overall, DEF is demonstrated as a quantitative metric to distinguish formulation dependent coning behavior and severity.

PMID 43008959
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PubMedMaterials today. Bio2026-11-08

An ibuprofen-eluting electrospun membrane prevents ureteral fibrosis by dampening macrophage-associated fibroblast activation.

Zhang Xi X, Zhong Da D, Xu Zihao Z, Li Yi Y et al.

Ureteral stricture is driven by unresolved inflammation and progressive matrix deposition, yet mechanism-guided local therapies remain limited. We integrated spatial transcriptomics of human normal and stricture ureters with an in-house scRNA-seq reference generated from three stricture specimens and independently evaluated annotation using the normal ureter dataset GSE194129. Urothelial injury-conditioned medium (UICM), primary ureteral fibroblasts, and THP-1-derived macrophages were used to model epithelial-immune-stromal signaling. An ibuprofen-functionalized PCL/gelatin electrospun membrane (P/G-PLL-IBU) was characterized and tested in a rabbit ureteral thermal-injury model. Spatial analysis identified a fibro-inflammatory niche with co-enrichment of fibroblast and macrophage programs in stenotic regions. Low normal-reference feature spots displayed cytoskeletal remodeling-associated signatures. UICM contained increased IL-6 and HMGB1 and elevated LDH release, induced an inflammatory fibroblast-like state, and produced a macrophage activation state dominated by pro-inflammatory features. Conditioned medium from UICM-activated macrophages enhanced FN1, COL1A1, α-SMA, and Smad2/3 phosphorylation in UICM-primed fibroblasts. Soluble ibuprofen suppressed macrophage NF-κB/COX-2-associated activation, and conditioned medium from treated cultures elicited lower profibrotic responses in fibroblasts. PGE2 add-back partially restored these responses. P/G-PLL-IBU preserved nanofibrous architecture, released ibuprofen for 56 days, and showed favorable hemocompatibility and cytocompatibility. In rabbits, P/G-PLL-IBU reduced early and long-term collagen deposition and upper urinary tract dilation for up to 90 days. Delayed membrane placement produced no detectable reversal of established fibrosis within the 30-day post-treatment observation window. Together, human spatial mapping and stepwise in vitro analyses link macrophage activation to fibroblast Smad2/3-associated remodeling in ureteral stricture, and local ibuprofen delivery via an electrospun membrane can blunt this trajectory after ureteral injury.

PMID 42997115
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PubMedEuropean heart journal. Case reports2026-11-06

Acute chest pain in an elite rugby player: a case report of polyserositis with cardiac involvement.

Betz Theresa Maria TM, Blank Norbert N, Zylla Maura Magdalena MM, Friedmann-Bette Birgit B

The evaluation of chest pain is a common reason for athletes to seek consultation at a sports medicine clinic. Musculoskeletal causes are by far most frequent; however, rare and potentially life-threatening aetiologies must also be considered. A 22-year-old professional rugby player presented with pleuritic chest pain for 2 weeks. Physical examination was unremarkable except for reduced breath sounds at the left lung base. Laboratory testing demonstrated marked systemic inflammation with a C-reactive protein level of 237 mg/L and mildly elevated high-sensitivity troponin T (21 pg/mL). Transthoracic ultrasound identified a fibrinous left-sided pleural effusion and a mild circumferential pericardial effusion. Subsequent cardiac magnetic resonance imaging (CMRI) confirmed the diagnosis of acute pericarditis. Comprehensive rheumatological evaluation established an autoimmune aetiology, consistent with a polyserositis secondary to mixed connective tissue disease (anti-nuclear antibody 1:80.000, speckled pattern, anti-RNP positive). Anti-inflammatory therapy with ibuprofen, colchicine and a corticosteroid pulse were initiated, resulting in clinical improvement and gradual normalization of laboratory and sonographic imaging findings within 6 weeks. After 3 months of sports restriction, follow-up CMRI demonstrated significant pericardial late gadolinium enhancement but without evidence of active inflammation. A gradual return-to-exercise protocol was subsequently implemented. Anti-inflammatory medication was discontinued after 6 months. The athlete has since remained clinically stable under regular follow-up for 1 year. This case highlights the importance of thorough diagnostic evaluation of chest pain in young athletes, including consideration of autoimmune causes such as polyserositis. Despite structured follow-up, uncertainty persists regarding recurrence risk and its significance for long-term athletic participation.

PMID 42992081
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PubMedColloids and surfaces. B, Biointerfaces2026-11-05

A pH-induced oral polymeric micelle containing ibuprofen for treating pediatric fever: a sustained-release strategy for extended antipyresis.

Liu Lingbo L, Wang Minjie M, Liu Wei W, Qin Shan S et al.

This study successfully constructed an ibuprofen (IBU)-loaded polymeric micelle system based on low-acetyl-content hydroxypropyl methylcellulose acetate succinate (HPMCAS-LG), designated as IBU/HPMCAS-LG, for efficient oral delivery and prolonged antipyretic effect. The polymeric micelles, prepared via acid-base neutralization, exhibited a small particle size (16.60 nm), a low PDI (0.230), and a low critical micelle concentration (CMC) (0.64 μmol/L), indicating excellent thermodynamic stability. In vitro release studies showed sustained, controlled release under simulated gastrointestinal pH conditions, with an 83.6% cumulative release at 24 h, superior to the medium (MG) and high (HG) acetyl content HPMCAS grades. Pharmacokinetic studies revealed a time to reach maximum concentration (tmax) of 0.5 h, a maximum plasma concentration (Cmax) of 138.53 μg/mL, an area under the curve (AUC0-t) of 576.18 μg·h/mL, a relative bioavailability of 134.5% relative to the commercial Motrin® suspension, and a mean residence time (MRT0-t) of 7.23 h. Compared with Motrin®, IBU/HPMCAS-LG showed a 57.3% higher Cmax, a 34.5% greater AUC0-t, and a 49% longer MRT0-t.In a yeast-induced pyretic rat model, IBU/HPMCAS-LG maintained normal body temperature for 14 h, significantly longer than Motrin® (10 h). Histological evaluation showed no obvious gastrointestinal mucosal damage after 7-day high-dose administration. These advantages are attributed to the polymeric micellar carrier's solubilizing effect, which maintains IBU in a molecularly dispersed state; its dense hydrophobic core and hydrogen-bonding network, which enable stable drug encapsulation and sustained release; and its pH-responsive behavior, which prolongs in vivo efficacy. Overall, IBU/HPMCAS-LG polymeric micelles represent a promising oral delivery system for poorly soluble drugs.

PMID 42987721
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