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infliximab (BCD055 / infliximab, Biocad)

✓ Approved

Grupo Biotoscana · TNF · Monoclonal Antibodies

What is infliximab?

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

Drug Profile

Brand NamesBCD055, infliximab, Biocad
CompanyGrupo Biotoscana
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
Musculoskeletal and connective tissue disordersAnkylosing spondylitis✓ Approved
Gastrointestinal disordersColitis ulcerative✓ Approved
Gastrointestinal disordersCrohn's disease✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved
Musculoskeletal and connective tissue disordersPsoriatic arthropathy✓ Approved

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Related Research Articles

PubMedFrontiers in immunology2026-10-22

Vitiligo onset following anti-inflammatory biological therapy: a scoping review.

Romagnuolo Maurizio M, Moltrasio Chiara C, Rossi Luisa Carlotta LC, Tavoletti Gianluca G et al.

Vitiligo is a chronic autoimmune depigmentation skin disorder characterized by the acquired loss of melanocytes, with a complex multifactorial pathophysiology. Among the potential predisposing factors, some drugs, including monoclonal antibodies, have been associated to disease onset. The aim of the present review is to summarize and discuss current literature findings in de novo vitiligo following biological targeting inflammatory cytokines. Overall, 18 articles were considered eligible for the present review, and details of demographics, clinical characteristics, vitiligo type and localization, biological drug administered and treatment outcomes were reported.The mean age of the 39 patients was 43 years (±16.3), with a male predominance (62%). Tumor necrosis factor-alpha (TNFα) inhibitors (infliximab, adalimumab, certolizumab pegol) were the most frequent suspected drugs (>50% of patients), followed by anti-IL-17A (ixekizumab, secukinumab) and anti-IL-12/23 (ustekinumab). Four cases were linked to anti-IL-4/13 (dupilumab). The median onset of vitiligo was 5 months post-initiation (range 1.5-24), with one-third of cases involving the face and neck, and two cases of segmental vitiligo. Biologic discontinuation or switching occurred in 26% of cases. Regarding outcomes, 41% experienced stabilization, 36% achieved varying degrees of repigmentation, and 8% progressed. While de novo vitiligo is reported as a potential adverse event of biological therapies, evidence for a direct causal relationship remains weak, with cases involving non-anti-TNFα agents appearing anecdotal. The co-occurrence of underlying autoimmune comorbidities in these patients points towards a coincidental rather than a causal relationship, highlighting the need for further research to fully elucidate this association.

PubMedJournal of medical case reports2026-10-21

Superior sagittal sinus thrombosis with intracranial hemorrhage in a patient on infliximab: a case report.

Alam Mohammad Rizwan MR, Corona-Ruiz Juan J, Cahill Joseph J, Goldsmith William W et al.

Superior sagittal sinus thrombosis (SSST) is a rare but life-threatening form of cerebral venous thrombosis. Although several prothrombotic and autoimmune conditions are recognized risk factors, SSST occurring in patients with rheumatoid arthritis (RA) receiving tumor necrosis factor-alpha (TNF-α) inhibitor therapy remains exceptionally rare and poorly described in the literature. We present a 59-year-old Caucasian female with RA treated with infliximab who developed extensive superior sagittal sinus thrombosis with concurrent intracranial and subarachnoid hemorrhage. The patient was managed with anticoagulation, blood pressure control, and seizure prophylaxis, with subsequent clinical and radiologic improvement at one-month follow-up. Hypercoagulability evaluation was overall unrevealing, and no other clear provoking etiology was identified. Given the rarity of this presentation, we report this case to raise awareness of a possible association between cerebral venous thrombosis and TNF-α inhibitor therapy in patients with rheumatoid arthritis. This is especially important given the increasing and widespread use of biologic agents in the treatment of autoimmune diseases.

PubMedJournal of the American Academy of Dermatology2026-10-20

Joint American Academy of Dermatology-Hidradenitis Suppurativa Foundation guidelines of care for the management of hidradenitis suppurativa.

Naik Haley B HB, Yeung Howa H, Frazer-Green Lindsy L, Daveluy Steven Daniel SD et al.

Hidradenitis suppurativa affects 0.7% to 1.5% of the global population and causes substantial disability and meaningfully impairs quality of life. To provide evidence-based recommendations for the management of hidradenitis suppurativa. A workgroup conducted a systematic review and applied the Grading of Recommendations, Assessment, Development, and Evaluation approach to assess the certainty of evidence and to develop recommendations. This guideline presents 37 evidence-based recommendations. Strong recommendations are made for adalimumab, bimekizumab, infliximab, secukinumab, and routine pain assessment. Conditional recommendations are made for topical clindamycin, resorcinol, and ruxolitinib; oral doxycycline, tetracycline, and clindamycin with rifampin; intravenous ertapenem; spironolactone; short-term systemic corticosteroids; upadacitinib; specific procedural interventions; tobacco cessation; supportive pain management; and zinc supplementation and vitamin D repletion. Analysis is limited to best evidence available from systematic review. These guidelines provide evidence-based recommendations for the management of hidradenitis suppurativa.

PubMedRheumatology (Oxford, England)2026-10-20

Activated B cells steer fibroblasts towards a proinflammatory phenotype in giant cell arteritis.

Xu Shuang S, Jiemy William F WF, Inrueangsri Nanthicha N, Ko YouBeen Y et al.

Giant cell arteritis (GCA) is characterized by chronic large-vessel inflammation and remodelling. Within affected arteries, especially in aorta, organized B cell clusters are mainly localized in adventitia, where fibroblasts represent the dominant stromal population. This study aims to investigate fibroblast heterogeneity within these clusters and B cell-fibroblast interactions in vitro as possible contributors to disease chronicity in GCA. Fibroblast phenotypes in CD20+B cell clusters in GCA and atherosclerotic aortic tissues were characterized using immunohistochemistry for fibroblast markers (CD90, PDPN, FAP, CD248, α-SMA) and cytokine expression (IL-6, GM-CSF, BAFF). In vitro, peripheral blood B cells from treatment-naïve GCA patients and healthy donors were stimulated and cocultured with human aortic adventitial fibroblasts (HAoAFs) using either direct cell coculture or transwell systems. To identify relevant molecular pathways for B cell-fibroblast interaction, HAoAFs were pre-treated with infliximab, tocilizumab, baricitinib or upadacitinib, followed by exposure to activated B cell conditioned medium (aBCCM). Protein secretion was assessed by ELISA, Luminex and Olink, mRNA expression was determined by qPCR. CD90+PDPN+immunofibroblasts mainly localized centrally, whereas CD90+FAP+ and CD90+CD248+fibroblasts mostly located at the border of the clusters. Fibroblasts in/around clusters co-expressed IL-6, GM-CSF, and BAFF. In vitro, HAoAFs cocultured with activated B cells or supernatants thereof upregulated IL-6, GM-CSF, PDPN, and FAP mRNA, and actively secreted IL-6, GM-CSF and BAFF, while type I collagen expression was suppressed. JAK-STAT inhibition abrogated these pro-inflammatory effects, whereas TNF-α and IL-6 receptor blockade did not. Activated B cells drive fibroblasts toward a pro-inflammatory phenotype, potentially sustaining chronic inflammation and disease progression in GCA. JAK-STAT signalling appears central to this effect, highlighting its therapeutic potency at the vascular level in GCA.

PubMedInflammatory bowel diseases2026-10-20

Large-scale proteomics identifies a pretreatment Crohn's disease core proteome and a dynamic signature for anti-TNF response.

Karns Rebekah R, Hyams Jeffrey S JS, Boyle Brendan M BM, Noe Joshua D JD et al.

With modest rates of endoscopic remission to anti-TNF biologics in children with moderate-to-severe Crohn's disease (CD), there is a critical need to develop noninvasive biomarkers associated with anti-TNF response. We performed a comprehensive proteomic evaluation to identify peripheral-blood candidate biomarkers for anti-TNF response. The ENvISION study enrolled patients (2-19 years old) with CD prior to starting infliximab or adalimumab with outcomes prospectively monitored at Month 3 (M3) and Month 12 (M12). The SomaScan® (Somalogic, Boulder, CO, 7322 analytes) was performed prior to anti-TNF treatment (baseline) at M3 and M12. Endoscopic remission was assessed at M12 (simple endoscopic score-CD < 3). Eighty patients with CD were enrolled with the CD Core Proteome developed from 61 prednisone-naive CD and 30 healthy controls. We identified 2999 differentially abundant proteins, 1403 with lower abundance and 1596 with higher abundance (FDR < 0.05). The CD Core Proteome was then compared across the three timepoints (baseline, M3 and M12) and we found that at both M3 and M12, the Core Proteome dysregulation retains strong identity with the baseline protein signal (β = .7, P < .001; β = .63, P < .001, respectively). Although the proteome exhibits change over time, it does not revert to a control-like state; rather, it transitions to a distinct "treated CD" proteome. In an exploratory investigation of the change in (delta) protein abundance from baseline to M3, we identified 132 proteins nominally associated with M12 endoscopic remission (P < .01). Using elastic net regression, we identified a three-protein panel (IRF1, NEUROG1, and APOA5) associated with M12 endoscopic remission (AUROC 0.94, 95% CI 0.88-1.0). In an exploratory investigation, we identified a CD Core Proteome and three-protein panel whose early changes were associated with M12 endoscopic remission, supporting their use as early pharmacodynamic response markers following external validation.

PubMedCurrent gastroenterology reports2026-10-18

Switching from Intravenous to Subcutaneous Infliximab in Children with Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis.

Spencer Elizabeth A EA

Subcutaneous infliximab (IFX-SC; CT-P13 SC/infliximab-dyyb/Remsima-SC/Zymfentra) is an approved maintenance option after intravenous (IV) induction in adults with inflammatory bowel disease (IBD), but it is not approved for patients < 18 years, and the pediatric evidence remains dispersed across small, largely observational cohorts. This review synthesizes the published pediatric experience of transitioning from IV to SC infliximab, examining maintenance of remission, drug concentrations, safety, and acceptability, and situates it within the adult evidence base and the distinctly pediatric concerns of access and dosing. A systematic search (PROSPERO: CRD420261465026) identified six independent, non-overlapping pediatric switch cohorts (n = 173). Random-effects proportional meta-analysis yielded pooled treatment persistence of 92% (95%CI 84-98), maintained clinical remission of 93% (95%CI 84-99), and any-cause discontinuation of 8% (95%CI 2-16), most often for injection-site intolerance, disease relapse, or paradoxical dermatitis. New anti-drug antibody formation was rare among the 129 children in cohorts measuring immunogenicity (four children, none sustained) while previously positive antibodies frequently resolved after switching. Steady-state SC concentrations ran roughly 2-fold above prior IV troughs, an expected step-up reflecting sustained subcutaneous exposure. Patient and caregiver satisfaction was high due to decreased school absence and travel, and cost analyses signaled net savings from avoided infusion-center use. The principal barrier was administrative: age-based denial. In appropriately selected children, transition to IFX-SC sustains remission with predictable pharmacokinetics, a reassuring immunogenicity profile, and excellent tolerability, mirroring the adult experience. These observations constitute a well-supported real-world signal and warrant prospective validation and pursuit of pediatric labeling.

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