Remicade

PANTS is a UK-wide, multicentre, prospective observational cohort study reporting the treatment failure rates of the anti-TNF drugs infliximab (originator, Remicade [Merck Sharp & Dohme] and biosimilar, CT-P13 [Celltrion]), and adalimumab (Humira [AbbVie]) in 1610 anti-TNF naive CD patients. The study design has been described in detail previously.^{8 (link),22 (link)} In brief, patients were recruited at the time of first anti-TNF exposure between February 2013 and June 2016, and evaluated for 12 months or until drug withdrawal. Eligible patients were aged ≥6 years with evidence of active luminal CD involving the colon and/or small intestine. Four major study visits were scheduled at week 0 [baseline], week 14 [post-induction], week 30, and week 54. Additional visits were scheduled at treatment failure or study exit. At baseline, clinical and demographic data were recorded, including sex, ethnicity, BMI, smoking status, age at diagnosis, disease duration, Montreal classification, prior medical and drug history, and previous CD-related surgeries. At every visit, disease activity score, weight, current therapy, and adverse events were recorded.^{8 (link)}

The rats were randomly distributed into four groups: the control, control+infliximab, hyperammonemic, and hyperammonemic+infliximab group. Infliximab is an anti-TNF-a antibody that does not cross the blood-brain barrier [40 (link)], binds to peripheral TNF-a, and reduces peripheral inflammation in rats with MHE or hyperammonemia [9 (link), 10 (link), 22 ]. Infliximab (Remicade; Merck Sharp & Dohme, Spain) was dissolved in saline (0.9% sodium chloride) and administered by i.v. injection (5 mg/kg) in the tail vein as described previously [41 (link)]. The first administration of infliximab was performed 2 days before the start of the ammonium-containing diet, and injections were repeated weekly for 4 weeks. Control rats were injected i.v. with saline. At the end of the 4th week, the rats were sacrificed by perfusion for in vivo immunohistochemical analysis of microglial and astrocyte activation (blue box), the protein expression of nuclear NF-kB and TNF-a in glia and Purkinje neurons (green box), and the mRNA expression of TNF-a in glia and Purkinje neurons (violet box) in the cerebellum (Fig. 1a).