P=N/A, N=90, Recruiting, University of Glasgow

Advanced therapies-particularly TNFα inhibitors-appear effective and well tolerated for severe or refractory DCS. Earlier initiation of treatment may help modify the inflammatory disease course and potentially prevent irreversible scarring alopecia; however, this proposed benefit remains hypothesis-generating and warrants prospective validation.

CD19 expression may be diminished by exams using a tafasitamab-competitive-binding clone. This case highlights not only the concern of HBV reactivation, but also the diagnostic challenge due to CD19 epitope masking following tafasitamab therapy.

Etanercept might be contemplated for "off-label" use in gout patients who do not respond to standard therapy or glucocorticoid therapy, encounter severe side-effects and contraindications.

Glial fibrillary acidic protein mRNA expression, a marker of astrocyte activation, was higher in the infliximab-treated APOE4-knockin with periodontitis group than in the control group. These suggest that APOE4 with periodontitis worsens neuronal loss and renal and hepatic fibrosis, and TNF-α inhibition in this coexistence may have harmful effects on both the brain and kidney.

During treatment, 3 patients (5%) developed transient rashes, with no treatment discontinuation required. HS016 exhibits significant efficacy and an acceptable safety profile in biologic-naïve PFCD patients, though the incremental maintenance strategy shows limited efficacy.

Beyond protein degradation, the diverse biological activities of thalidomide are discussed, including modulation of cytokines, angiogenesis, and immune signaling pathways. Collectively, thalidomide exemplifies how mechanistic insight, synthetic innovation and careful risk-benefit evaluation can transform a once-discarded molecule into a cornerstone of contemporary drug design.

P=N/A, N=23900, Completed, Takeda | Not yet recruiting --> Completed

P2, N=120, Active, not recruiting, Johns Hopkins University | Recruiting --> Active, not recruiting

P3, N=49, Active, not recruiting, UCB Biopharma SRL | Trial completion date: Aug 2034 --> Jul 2026 | Trial primary completion date: Sep 2029 --> Apr 2026

While approved pan-FGFR inhibitors provide clinical benefit, their durability is limited by acquired, often polyclonal, on-target resistance mutations affecting key regions of the FGFR2 kinase domain, including the gatekeeper residue (V565), molecular brake residues (N550, E566, K642), and other key variants...Given FGFR2-associated toxicities and the need for subtype selectivity, FGFR4 inhibition was prioritized as a selectivity determinant, while sparing FGFR1 was considered less critical. Guided by structure-based drug design, a reversible aminopyrimidine screening hit was optimized into a novel covalent inhibitor series active against FGFR2 wild-type and clinically relevant resistance mutations. An advanced lead 13 showed favorable potency, ADME properties, and demonstrated proof-of-concept in vivo efficacy in an FGFR2-amplified xenograft model comparable with the standard of care.

P=N/A, N=881, Active, not recruiting, Celltrion | Recruiting --> Active, not recruiting