Nanjing Shunxin Pharmaceutical · TNF · Monoclonal Antibodies
adalimumab is a monoclonal antibodies developed by Nanjing Shunxin Pharmaceutical. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.
| Brand Names | Taibowei, TQZ2301, Tabovi |
| Company | Nanjing Shunxin Pharmaceutical |
| Drug Class | Monoclonal Antibodies, Antibody |
| Molecular Target | TNF |
| Route | Injectable (Others), Subcutaneous Injection |
| Status | Approved |
adalimumab acts on 1 molecular target:
| TNF | tumor necrosis factor (TNFA, TNF-alpha) |
adalimumab is developed for 10 unique indications across 4 therapeutic areas.
| Therapeutic Area | Condition | Phase |
|---|---|---|
| Musculoskeletal and connective tissue disorders | Ankylosing spondylitis | ✓ Approved |
| Gastrointestinal disorders | Crohn's disease | ✓ Approved |
| Skin and subcutaneous tissue disorders | Psoriasis | ✓ Approved |
| Musculoskeletal and connective tissue disorders | Rheumatoid arthritis | ✓ Approved |
| Eye disorders | Uveitis | ✓ Approved |
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Sign up free to view all indications →Gawari Nitin Chintaman NC, Naik Tanvi T, Shingare Sujata Prakash SP, Hassan Yasir Y
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.
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.
Algov Itay I, Shue Lawrence L, Zhou Xin X
Soluble extracellular proteins drive many physiological and pathological signaling pathways, and targeted degradation offers a potential strategy for their therapeutic modulation. Here, we engineered bispecific targeting chimeras (TACs) that couple soluble proteins to constitutively internalizing cell-surface effectors for clearance. Using transferrin receptor 1 (TfR1) as an initial effector, we find that uptake depends on both binding arms. Rapid target association facilitates extracellular antigen capture, while increased intracellular dissociation can improve uptake when overall binding strength is maintained. Introducing pH-sensitive target binders enhances internalization, but only when neutral-pH affinity remains high. We also find that atypical chemokine receptor 5 (ACKR5) can serve as an alternative internalizing effector. Applying these principles to tumor necrosis factor-alpha (TNF-α), an optimized TAC more effectively inhibits its signaling than FDA-approved anti-TNF-α therapy adalimumab. These findings identified molecular determinants for engineering TACs targeting soluble extracellular proteins.
Amar Yacine Y, Baumann Diana D, Niedermeier Sebastian S, Silva Rafaela L RL et al.
Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease with a multifactorial pathogenesis involving genetic, lifestyle and microbial factors. While cutaneous microbiome shifts have been reported for this disease, the impact of systemic immunomodulators and antibiotics on HS microbiome remains poorly defined. To characterize species-level cutaneous dysbiosis in HS and evaluate the effects of three standard-of-care systemic therapies, clindamycin/rifampicin (ATB), adalimumab (ADA) and secukinumab (SEC) on skin microbial composition. We performed 16S rRNA sequencing on 251 skin swabs from lesional and non-lesional sites of 52 HS patients and 31 healthy matched controls. In a sub-cohort of 28 patients, microbial shifts were evaluated following 12 weeks of therapy with ATB (n = 8), ADA (n = 12) and SEC (n = 8). HS skin exhibited profound dysbiosis defined by the depletion of homeostatic commensals (Cutibacterium acnes, Staphylococcus hominis, S. epidermidis) and a synergistic expansion of anaerobic pathogens, primarily Gram-positive anaerobic cocci (GPAC; Finegoldia magna, Peptoniphilus grossensis and Fenollaria massiliensis), Lawsonella clevelandensis and Campylobacter ureolyticus. A 13-taxa microbial signature accurately discriminated the HS phenotype (AUC = 0.92). Following 12 weeks of treatment, ATB markedly attenuated dysbiosis by reducing pathogen loads and significantly increasing microbial richness. In contrast, ADA and SEC did not alter pathogen abundance and were associated with a slight decline in protective commensals. Systemic antibiotics partially restore cutaneous microbiome homeostasis in HS by targeting anaerobic pathogens while preserving beneficial commensals, an effect not observed with the tested biologics. These findings highlight the need for microbiome-directed adjuvant therapies to complement immunomodulation in HS management.
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.
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