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Previous exposure to TNF inhibitors other than Humira was permitted in up to 25% of patients

In rodents, enteral administration of acetate and butyrate has been shown to induce the expression of beta-defensin and histone inhibitor-related antimicrobial peptides in intestinal epithelial cells in a GPR43-mediated manner as a means of protecting the intestinal barrier and organizing the inflammatory response induced by, among others, LPS (173)

The result of the loss of these proteins from the cell surface increases sensitivity to complement-mediated cell destruction

Importantly, targeting of MK-801 to GLP-1 receptor-expressing brain regions circumvents adverse physiological and behavioural effects associated with MK-801 monotherapy