The Muscleblind Like-Proteins (MBNL) are key regulators of precursor and mature mRNA metabolism in mammals. MBNL is involved in 80% of mechanisms regulating the multisystemic effects of DM1. Accordingly, by increasing MBNL at least 80% of the collateral effects of the disease will be ameliorated.

See for further details about the different symptoms associated to DM.

MBNL1 is the best-studied family member of MBNL proteins due to its predominant expression in muscle tissue, as well as in brain, heart and liver. It is also a regulator of alternative splicing. Hundreds of alternative exons have their processing altered in DM1 and some of them correlate directly with the symptoms of DM1[4]. In fact, MBNL1 functional decrease is the key element in DM pathogenesis[5]. It has been disclosed that functional down-regulation of MBNLs in human causes adult-to-fetal alternative splicing transition.

According to data obtained by Myogem Health Company from the in vitro and in vivo experiments performed by Dr. Artero and Dr. Llamusí of the Translational Genomics Group of the University of Valencia, Myo-DM has demonstrated its ability to increase The levels of MBNL expression, both MBNL1 and MBNL2 and their effective amount in nucleus of human DM1 myoblast. In fact, the ingredients of Myo-DM, the xanthines caffeine and theobromine, have been formulated to the composition and optimal doses to maximize the amount of MBNL in the nuclei of this cell type.


[4] Wang et al, Antagonistic regulation of mRNA expression and splicing by CELF and MBNL proteins, Genome Res. 2015 Jun;25(6):858-71. doi: 10.1101/gr.184390.114. Epub 2015 Apr 16.
[5] Konieczny, P. et al. MBNL proteins and their target RNAs, interaction and splicing regulation. Nucleic Acid Research, 2014, 42 (17), 10873-10887.