Dirucotide (MBP 8298) is a synthetic myelin basic protein (MBP) peptide designed to decrease type 2 helper T cells (TH2)-mediated B-cell signalling of auto-reactive T-cells thereby reducing the production of specific antibodies that target endogenous MBP. MBP is the dominant site of attack in patients with multiple sclerosis and haplotype (HLA) DR2 or DR4. Dirucotide did not meet the primary endpoint of delaying disease progression, as measured by the Expanded Disability Status Scale (EDSS), during the two-year MAESTRO-01 Phase III trial in patients with secondary progressive multiple sclerosis (SPMS). In addition, there were no statistically significant differences between dirucotide and placebo on the secondary endpoints of the study. After disappointing trial results, development of the drug was ended in 2009.

Disitertide (P144) is a TGF-β1 antagonist peptide. Disitertide prevents TGF-β1-dependent inhibition of MV1Lu proliferation in vitro and markedly reduces binding of TGF-β1 to its receptors. P144 blocked TGF-beta1-dependent stimulation of a reporter gene under the control of human alpha2(I) collagen promoter. Intraperitoneal administration of P144 also showed potent antifibrogenic activity in vivo in the liver of rats receiving CCl4. These rats also showed a significant decrease in the number of activated hepatic stellate cells as compared with those treated with saline only. P144 decreased proliferation, migration, invasiveness, and tumorigenicity in vitro, whereas apoptosis and anoikis were significantly increased for glioblastoma cell lines. SMAD2 phosphorylation was reduced, together with a downregulation of SKI and an upregulation of SMAD7 at both transcriptional and translational levels. Additionally, P144 was able to impair tumor growth and increase survival in an in vivo flank model. This findings suggest a potential effect of P144 in vitro and in vivo that is mediated by regulation of transcriptional target genes of the TGF-β pathway, suggesting a therapeutic potential of P144 for glioblastoma treatment. Topical application of disitertide may promote scar maturation and clinical improvement of hypertrophic scar morphology features in an "in vivo" model in nude mice after two weeks of treatment.