target the dux4 mrna, including altering splicing or polyadenylation; block the activity of the dux4 protein inhibit the dux4-induced process, or processes, that leads to pathology. small molecule drugs most drugs used in medicine are "small molecule drugs," as opposed to biologic medical products that include proteins, vaccines, and nucleic acids. small molecule drugs can typically be taken by ingestion, rather than injection. losmapimod, a selective inhibitor of p38α/β mitogen-activated protein kinases, was identified by fulcrum therapeutics as a potent suppressor of dux4 in vitro. results of a phase iib clinical trial, revealed in june 2021, showed statistically significant slowing of muscle function deterioration. further trials are pending. casein kinase 1 (ck1) inhibition has been identified by facio therapies, a dutch pharmaceutical company, to repress dux4 expression and is in preclinical development. facio therapies claims that ck1 inhibition leaves myotube fusion intact, unlike bet inhibitors, p38 mapk inhibitors, and β2 agonists. gene therapy gene therapy is the administration of nucleotides to treat disease. multiple types of gene therapy are in the preclinical stage of development for the treatment of fshd. antisense therapy utilizes antisense oligonucleotides that bind to dux4 messenger rna, inducing its degradation and preventing dux4 protein production. phosphorodiamidate morpholinos, an oligonucleotide modified to increase its stability, have been shown to selectively reduce dux4 and its effects; however, these antisense nucleotides have poor ability to penetrate muscle. micrornas (mirnas) directed against dux4, delivered by viral vectors, have shown to reduce dux4, protect against muscle pathology, and prevent loss of grip strength in mouse fshd models. arrowhead pharmaceuticals is developing an rna interference therapeutic against dux4, named aro-dux4, and intends to file for regulatory clearance in third quarter of 2021 to begin clinical trials. genome editing, the permanent alteration of genetic code, is being researched. one study tried to use crispr-cas9 to knockout the polyadenylation signal in lab dish models, but was unable to show therapeutic results. potential drug targets inhibition of the hyaluronic acid (ha) pathway is a potential therapy. one study found that many dux4-induced molecular pathologies are mediated by ha signaling, and inhibition of ha biosynthesis with 4-methylumbelliferone prevented these molecular pathologies. p300 inhibition has shown to inhibit the deleterious effects of dux4 bet inhibitors have been shown to reduce dux4 expression. antioxidants could potentially reduce the effects of fshd. one study found that vitamin c, vitamin e, zinc gluconate, and selenomethionine supplementation increased endurance and strength of the quadriceps, but had no significant benefit on walking performance. further study is warranted. outcome measures ways of measuring the disease are important for studying disease progression and assessing the efficacy of drugs in clinical trials. quality of life can be measured with questionnaires, such as the fshd health index. how the disease affects daily activities can measured with questionnaires, such as the fshd‐rasch‐built overall disability scale (fshd-rods) or fshd composite outcome measure (fshd-com). electrical impedance myography is being studied as a way to measure muscle damage. muscle mri is useful for assessment of all the muscles in the body. muscles can be scored based on the degree of fat infiltration.