in vitro but did not make it to the clinical stage include growth hormone, various histone deacetylase inhibitors, benzamide m344, hydroxamic acids (cbha, sbha, entinostat, panobinostat, trichostatin a, vorinostat), prolactin as well as natural polyphenol compounds like resveratrol and curcumin. celecoxib, a p38 pathway activator, is sometimes used off-label by people with sma based on a single animal study but such use is not backed by clinical-stage research. smn stabilisation smn stabilisation aims at stabilising the smnδ7 protein, the short-lived defective protein coded by the smn2 gene, so that it is able to sustain neuronal cells. no compounds have been taken forward to the clinical stage. aminoglycosides showed capability to increase smn protein availability in two studies. indoprofen offered some promise in vitro. neuroprotection neuroprotective drugs aim at enabling the survival of motor neurons even with low levels of smn protein. olesoxime was a proprietary neuroprotective compound developed by the french company trophos, later acquired by hoffmann-la roche, which showed stabilising effect in a phase-ii clinical trial involving people with sma types 2 and 3. its development was discontinued in 2018 in view of competition from nusinersen and underwhelming data from an open-label extension trial. of clinically studied compounds which did not show efficacy, thyrotropin-releasing hormone (trh) held some promise in an open-label uncontrolled clinical trial but did not prove effective in a subsequent double-blind placebo-controlled trial. riluzole, a drug that offers limited clinical benefit in amyotrophic lateral sclerosis, was proposed to be similarly tested in sma; however, a 2008–2010 trial in sma types 2 and 3 was stopped early due to the lack of satisfactory results. other compounds that displayed some neuroprotective effect in in vitro research but never moved on to in vivo studies include β-lactam antibiotics (e.g., ceftriaxone) and follistatin. muscle restoration this approach aims to counter the effect of sma by targeting the muscle tissue instead of neurons. reldesemtiv (ck-2127107, ck-107) is a skeletal troponin activator developed by cytokinetics in cooperation with astellas. the drug aims at increasing muscle reactivity despite lowered neural signalling. the molecule showed some success in phase ii clinical trial in adolescent and adults with sma types 2, 3, and 4. apitegromab (srk-015) is monoclonal antibody that blocks the activation of the skeletal muscle protein myostatin, thereby promoting muscle tissue growth. as of 2021, the molecule showed success as an experimental add-on treatment in paediatric and adult patients treated with nusinersen. gym329 (ro7204239), developed by hoffman-la roche, works similarly to apitegromab by blocking myostatin activation. as of 2022, it is undergoing clinical development in non-ambulant children with sma aged 2–10, combined with risdiplam. stem cells whilst stem cells never form a part of any recognised therapy for sma, a number of private companies, usually located in countries with lax regulatory oversight, take advantage of media hype and market stem cell injections as a "cure" for a vast range of disorders, including sma. the medical consensus is that such procedures offer no clinical benefit whilst carrying significant risk, therefore people with sma are advised against them. in 2013–2014, a small number of sma1 children in italy received court-mandated stem cell injections following the stamina scam, but the treatment was reported having no effect registries people with sma in the european union can participate in clinical research by entering their details into registries managed by treat-nmd.