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infliximab (infliximab, Epirus / BOW015 / Infimab)

✓ Approved

Ranbaxy Laboratories Limited · TNF · Monoclonal Antibodies

What is infliximab?

infliximab is a monoclonal antibodies developed by Ranbaxy Laboratories Limited. It is approved for therapeutic indications via injectable (others) or intraocular injection or intravenous (iv).

Drug Profile

Brand Namesinfliximab, Epirus, BOW015, Infimab
CompanyRanbaxy Laboratories Limited
Drug ClassMonoclonal Antibodies, Antibody
Molecular TargetTNF
RouteInjectable (Others), Intraocular Injection, Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

infliximab acts on 1 molecular target:

TNFtumor necrosis factor (TNFA, TNF-alpha)
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Therapeutic Indications

infliximab is developed for 7 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
Gastrointestinal disordersAnal fistula✓ Approved
Musculoskeletal and connective tissue disordersAnkylosing spondylitis✓ Approved
Gastrointestinal disordersColitis ulcerative✓ Approved
Gastrointestinal disordersCrohn's disease✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved

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Related Research Articles

PubMedClinical case reports2026-11-11

Infliximab for Refractory Diffuse Sclerosing Osteomyelitis of the Mandible Associated With Ulcerative Colitis: A Case Report.

Yao Mayumi M, Obata Kyoichi K, Takei Kensuke K, Miyake Yoshitaka Y et al.

Diffuse sclerosing osteomyelitis (DSO) of the mandible is a chronic nonbacterial inflammatory bone disease. We report a 65-year-old woman with ulcerative colitis who presented with swelling and pain of the left mandible. The lesion was refractory to tooth extraction, prolonged antibiotics, and nonsteroidal anti-inflammatory drugs. CT showed widespread loss of trabecular structure and osteosclerosis, and bone scintigraphy demonstrated abnormal uptake confined to the mandible, without findings suggestive of synovitis, acne, pustulosis, hyperostosis, and osteitis syndrome. DSO was diagnosed based on the overall clinical course, progressive radiological findings, persistence despite treatment of the suspected odontogenic foci and repeated antibiotic therapy, and supportive histopathological findings. Anti-tumor necrosis factor-α (TNF-α) therapy was considered for the refractory DSO, and infliximab was selected because it is also effective for ulcerative colitis; her symptoms resolved promptly, and imaging showed marked improvement with restoration of trabecular bone. No relapse or treatment-related adverse events occurred during 3 years of follow-up. The clinical and radiographic improvement observed following infliximab treatment in this older adult raises the possibility that TNF-α-mediated inflammatory pathways may be involved in refractory DSO associated with ulcerative colitis and supports further investigation of anti-TNF-α therapy in this setting.

PubMedEuropean journal of case reports in internal medicine2026-11-11

Pyoderma Gangrenosum and Haematochezia in A Patient with Previous Cocaine Abuse.

Hadjicharalambous Myrianthi M, Symeonidou Sofia S, Georgiou George G, Azina Chara C et al.

Pyoderma gangrenosum (PG) is an autoinflammatory neutrophilic dermatosis that may rarely occur in association with granulomatosis with polyangiitis (GPA). Management of refractory disease remains challenging. A 48-year-old man with a history of previous cocaine abuse was admitted due to impaired feeding in the context of a chronic hard palate perforation and a large oro-sinus fistula. During hospitalisation, he developed haematochezia and painful ulcerative skin lesions involving the right upper limb and lower extremities. Upper and lower gastrointestinal endoscopy revealed a Forrest IIc gastric lesion and a non-bleeding ileocecal ulcer. Histopathological examination of skin lesions demonstrated dense neutrophilic infiltration consistent with PG, while gastrointestinal biopsies excluded inflammatory bowel disease. An extensive evaluation excluded infection, antiphospholipid syndrome, cryoglobulinaemia, malignancy and vascular occlusive disease, all of which may mimic PG. Autoimmune screening workup yielded positive for anti-proteinase-3 antibodies (C-ANCA). The patient initially received high-dose methylprednisolone followed by mycophenolate mofetil and infliximab. Despite treatment, disease activity persisted with recurrent relapses, requiring hospitalisations. Upadacitinib was subsequently introduced, resulting in rapid clinical improvement, near-complete healing of skin lesions and successful glucocorticoid withdrawal. The coexistence of PG and GPA is rare and presents substantial diagnostic and therapeutic challenges. JAK inhibition with upadacitinib may represent a promising therapeutic option in refractory cases. Pyoderma gangrenosum may rarely coexist with granulomatosis with polyangiitis, creating significant diagnostic and therapeutic challenges.A history of cocaine abuse may complicate the diagnostic evaluation because cocaine-induced vasculitis can mimic ANCA-associated vasculitis.Upadacitinib may represent a promising steroid-sparing therapeutic option in refractory pyoderma gangrenosum associated with granulomatosis with polyangiitis.Pyoderma gangrenosum is a diagnosis of exclusion for which no confirmatory test exists; approximately 10% of patients given the diagnosis are subsequently found to have an alternative condition, so mimickers must be actively excluded before and during treatment.

PubMedInflammatory bowel diseases2026-11-10

Comparative effectiveness of infliximab and tofacitinib in advanced therapy-naive and -exposed patients with ulcerative colitis: a multicenter real-world study.

Mizuta Noboru N, Kinoshita Naohiko N, Kakimoto Kazuki K, Hara Azusa A et al.

and Aim: Infliximab (IFX) and tofacitinib (TOF) are advanced therapies for ulcerative colitis (UC), but real-world comparative data by prior advanced therapy (AT) exposure remain limited. We compared effectiveness by prior AT exposure. This multicenter retrospective cohort study included adults with UC who initiated IFX or TOF between June 2010 and May 2025. The primary analysis was restricted to May 2018 onward, when both were available in Japan. AT-naive and AT-exposed cohorts were analyzed separately using overlap weighting. The primary outcome was corticosteroid-free clinical remission at week 52. Of 266 patients (137 IFX, 129 TOF), the primary analysis included 76 AT-naive (27 IFX, 49 TOF) and 120 AT-exposed (40 IFX, 80 TOF) patients. Week 14 remission did not differ significantly between treatments in either cohort. At week 52, remission numerically favored TOF in AT-naive patients (IFX, 43.9%; TOF, 64.5%; odds ratio [OR], 2.32; 95% CI, 0.84-6.44; P = .105), whereas remission was higher with TOF in the AT-exposed cohort (IFX, 19.0%; TOF, 38.8%; OR, 2.71; 95% CI, 1.08-6.80; nominal P = .034). Three-year treatment persistence did not differ significantly in either cohort but numerically favored TOF in AT-naive patients (IFX, 39.2%; TOF, 61.5%; hazard ratio, 0.64; 95% CI, 0.31-1.36). Multiple-imputation analyses yielded similar findings. Week 52 remission numerically favored TOF in AT-naive patients and was higher with TOF in AT-exposed patients. Clinically relevant differences in 3-year persistence could not be ruled out, particularly in AT-naive patients. These findings are exploratory.

PubMedInflammatory bowel diseases2026-11-10

Epstein-Barr virus and inflammatory bowel disease: a systematic review of its clinical significance and potential pathogenic role.

Estevinho Maria Manuela MM, Said Hyder H, Nandy Anubhab A, Snapper Scott B SB et al.

Several studies report an association between Epstein-Barr virus (EBV) and inflammatory bowel disease (IBD). This review critically synthesizes current evidence on these association between EBV and IBD, its potential mechanisms, clinical implications, and research gaps. A systematic search identified studies investigating EBV in IBD using serological, molecular, and tissue-based approaches. Data on EBV prevalence, viral load, disease phenotype, treatment status, and clinical outcomes were extracted, and study quality was assessed. A narrative review examined proposed mechanisms that may potentially link EBV to intestinal inflammation. From 7271 citations, 45 studies met inclusion criteria. EBV was more frequently detected in intestinal tissue from IBD patients than in controls, particularly in active or refractory disease, whereas findings for seroprevalence and blood-based markers were less consistent. Some longitudinal studies reported associations between prior EBV exposure and subsequent IBD, particularly Crohn's disease, but these observations do not establish a causal relationship. Proposed mechanisms involving EBV-infected B cells, molecular mimicry, and altered cytokine signaling provide biological plausibility but remain unproven in IBD. EBV latency programs and age at seroconversion may influence disease progression and reactivation risk, although data remain limited. Corticosteroids and therapy with infliximab plus azathioprine have been associated with higher EBV loads, especially in refractory disease, yet these findings may be confounded by disease severity and treatment exposure. Current evidence supports an association between EBV and IBD, particularly in severe and refractory disease but does not establish-and equally does not exclude-a pathogenic role for EBV. Considerable methodological heterogeneity in study design and EBV detection methods and the observational nature of the available data limit causal interpretation. Prospective mechanistic studies are needed to determine whether EBV is a causal contributor, a disease modifier, or a marker of underlying immune dysregulation.

PubMedAutoimmunity reviews2026-11-09

TNF-inhibitors for Behcet's syndrome: past, present and future.

Sfikakis Petros P PP, Hatemi Gulen G

Herein we summarize data on the use of TNF inhibitors for Behcet's Syndrome (BS) published in past 25 years and discuss future perspectives. Anti-TNF monoclonal antibodies proved first efficacious for BS-associated sight-threatening panuveitis, resulting in a dramatic drop in current rates of blindness compared to the pre-anti-TNF era. In addition to ocular disease, their remarkable efficacy was subsequently documented in all clinical domains of BS, namely mucocutaneous, articular, vascular, gastrointestinal and central nervous system disease. To date TNF inhibitors have moved to the front line and most patients with vital organ involvement, including children, have been, or currently are under anti-TNF treatment. Moreover, large retrospective studies showed that both anti-TNF monoclonal antibodies Infliximab and Adalimumab reduced the emergence of new clinical manifestations of BS in most patients under treatment. Smaller studies have shown that, if successful, anti-TNF treatment can be discontinued after at least two years with half of patients remaining disease-free in the long term. These findings suggest that TNF inhibitors may modify BS natural history, however, a prospective international study of consecutive patients who start treatment for mucocutaneous or articular manifestations only, is needed. Thus, we debate on the earliest possible use of TNF inhibitors in severe BS, in order to achieve remission and perhaps preservation of vital organ function and quality of life. Although not demonstrated yet, this approach may also reduce mortality rates as has happened in other rheumatic diseases. We propose that every candidate drug for BS should be compared for efficacy and safety to TNF inhibitors.

PubMedCureus2026-11-08

Miliary-Pattern Pulmonary Tuberculosis During Infliximab Therapy Despite Negative Tuberculosis Screening.

Kenawi Adel A, Zahid Nomaan N, Humeda Mohammad M, Arbab Ahmed A et al.

Tumour necrosis factor-alpha (TNF-α) inhibition increases the risk of tuberculosis (TB), including disseminated and miliary disease. Although screening for latent TB is recommended before anti-TNF therapy, negative or indeterminate interferon-gamma release assay (IGRA) results do not exclude active TB, particularly in immunosuppressed patients. We report a 32-year-old man with ulcerative colitis who developed progressive respiratory and constitutional symptoms while receiving infliximab. He developed severe hypoxaemic respiratory failure requiring high-flow nasal oxygen. Chest imaging demonstrated diffuse miliary nodularity with bilateral ground-glass changes, consolidation, and mediastinal lymphadenopathy. Despite previous negative and subsequent indeterminate QuantiFERON-TB results, the clinical and radiological findings prompted empirical anti-tuberculous treatment while respiratory samples were obtained. Sputum culture subsequently grew Mycobacterium tuberculosis, while a Hain molecular assay and bronchial washing confirmed the M. tuberculosis complex. Infliximab was withheld, and the patient improved clinically, with respiratory support reduced from high-flow nasal oxygen to conventional oxygen. He subsequently reported symptomatic improvement during respiratory follow-up. This case highlights the limitations of TB screening tests in patients receiving anti-TNF therapy and demonstrates that a negative or indeterminate interferon-gamma release assay (IGRA) should not delay investigation for active TB when clinical and radiological features are strongly suggestive.

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