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'''Emrusolmin''' (development code '''Anle138b''') is an experimental drug for the treatment of neurodegenerative diseases. It is an inhibitor of protein aggregation, particularly preventing the aggregation of ] which is implicated in the development of ].<ref>{{cite journal | doi = 10.1007/s00401-013-1114-9 | title = Anle138b: A novel oligomer modulator for disease-modifying therapy of neurodegenerative diseases such as prion and Parkinson's disease | date = 2013 | vauthors = Wagner J, Ryazanov S, Leonov A, Levin J, Shi S, Schmidt F, Prix C, Pan-Montojo F, Bertsch U, Mitteregger-Kretzschmar G, Geissen M, Eiden M, Leidel F, Hirschberger T, Deeg AA, Krauth JJ, Zinth W, Tavan P, Pilger J, Zweckstetter M, Frank T, Bähr M, Weishaupt JH, Uhr M, Urlaub H, Teichmann U, Samwer M, Bötzel K, Groschup M, Kretzschmar H | journal = Acta Neuropathologica | volume = 125 | issue = 6 | pages = 795–813 | pmid = 23604588 | pmc = 3661926 }}</ref><ref>{{cite journal | doi = 10.1016/j.ymeth.2023.04.002 | title = Anle138b interaction in α-synuclein aggregates by dynamic nuclear polarization NMR | date = 2023 | vauthors = Dervişoğlu R, Antonschmidt L, Nimerovsky E, Sant V, Kim M, Ryazanov S, Leonov A, Fuentes-Monteverde JC, Wegstroth M, Giller K, Mathies G, Giese A, Becker S, Griesinger C, Andreas LB | journal = Methods | volume = 214 | pages = 18–27 | pmid = 37037308 }}</ref><ref>{{cite journal | doi = 10.1038/s41467-022-32797-w | title = The clinical drug candidate anle138b binds in a cavity of lipidic α-synuclein fibrils | date = 2022 | vauthors = Antonschmidt L, Matthes D, DervişOğLu R, Frieg B, Dienemann C, Leonov A, Nimerovsky E, Sant V, Ryazanov S, Giese A, Schröder GF, Becker S, De Groot BL, Griesinger C, Andreas LB | journal = Nature Communications | volume = 13 | issue = 1 | page = 5385 | pmid = 36104315 | pmc = 9474542 }}</ref> Other proteins it inhibits the aggregation of include ]<ref>{{cite journal | doi = 10.1007/s00401-015-1483-3 | title = Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies | date = 2015 | vauthors = Wagner J, Krauss S, Shi S, Ryazanov S, Steffen J, Miklitz C, Leonov A, Kleinknecht A, Göricke B, Weishaupt JH, Weckbecker D, Reiner AM, Zinth W, Levin J, Ehninger D, Remy S, Kretzschmar HA, Griesinger C, Giese A, Fuhrmann M | journal = Acta Neuropathologica | volume = 130 | issue = 5 | pages = 619–631 | pmid = 26439832 | pmc = 4612332 }}</ref> which is associated with ] (AD) and ], and ]<ref>{{cite journal | doi = 10.15252/emmm.201707825 | title = The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology | date = 2018 | vauthors = Martinez Hernandez A, Urbanke H, Gillman AL, Lee J, Ryazanov S, Agbemenyah HY, Benito E, Jain G, Kaurani L, Grigorian G, Leonov A, Rezaei-Ghaleh N, Wilken P, Arce FT, Wagner J, Fuhrman M, Caruana M, Camilleri A, Vassallo N, Zweckstetter M, Benz R, Giese A, Schneider A, Korte M, Lal R, Griesinger C, Eichele G, Fischer A | journal = EMBO Molecular Medicine | volume = 10 | pages = 32–47 | pmid = 29208638 }}</ref> which is associated with AD. '''Emrusolmin''' (development code '''Anle138b''') is an experimental drug for the treatment of neurodegenerative diseases. It is an inhibitor of protein aggregation, particularly preventing the aggregation of ] which is implicated in the development of ].<ref>{{cite journal | doi = 10.1007/s00401-013-1114-9 | title = Anle138b: A novel oligomer modulator for disease-modifying therapy of neurodegenerative diseases such as prion and Parkinson's disease | date = 2013 | vauthors = Wagner J, Ryazanov S, Leonov A, Levin J, Shi S, Schmidt F, Prix C, Pan-Montojo F, Bertsch U, Mitteregger-Kretzschmar G, Geissen M, Eiden M, Leidel F, Hirschberger T, Deeg AA, Krauth JJ, Zinth W, Tavan P, Pilger J, Zweckstetter M, Frank T, Bähr M, Weishaupt JH, Uhr M, Urlaub H, Teichmann U, Samwer M, Bötzel K, Groschup M, Kretzschmar H | journal = Acta Neuropathologica | volume = 125 | issue = 6 | pages = 795–813 | pmid = 23604588 | pmc = 3661926 }}</ref><ref>{{cite journal | doi = 10.1016/j.ymeth.2023.04.002 | title = Anle138b interaction in α-synuclein aggregates by dynamic nuclear polarization NMR | date = 2023 | vauthors = Dervişoğlu R, Antonschmidt L, Nimerovsky E, Sant V, Kim M, Ryazanov S, Leonov A, Fuentes-Monteverde JC, Wegstroth M, Giller K, Mathies G, Giese A, Becker S, Griesinger C, Andreas LB | journal = Methods | volume = 214 | pages = 18–27 | pmid = 37037308 }}</ref><ref>{{cite journal | doi = 10.1038/s41467-022-32797-w | title = The clinical drug candidate anle138b binds in a cavity of lipidic α-synuclein fibrils | date = 2022 | vauthors = Antonschmidt L, Matthes D, DervişOğLu R, Frieg B, Dienemann C, Leonov A, Nimerovsky E, Sant V, Ryazanov S, Giese A, Schröder GF, Becker S, De Groot BL, Griesinger C, Andreas LB | journal = Nature Communications | volume = 13 | issue = 1 | page = 5385 | pmid = 36104315 | pmc = 9474542 | bibcode = 2022NatCo..13.5385A }}</ref> Other proteins it inhibits the aggregation of include ]<ref>{{cite journal | doi = 10.1007/s00401-015-1483-3 | title = Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies | date = 2015 | vauthors = Wagner J, Krauss S, Shi S, Ryazanov S, Steffen J, Miklitz C, Leonov A, Kleinknecht A, Göricke B, Weishaupt JH, Weckbecker D, Reiner AM, Zinth W, Levin J, Ehninger D, Remy S, Kretzschmar HA, Griesinger C, Giese A, Fuhrmann M | journal = Acta Neuropathologica | volume = 130 | issue = 5 | pages = 619–631 | pmid = 26439832 | pmc = 4612332 }}</ref> which is associated with ] (AD) and ], and ]<ref>{{cite journal | doi = 10.15252/emmm.201707825 | title = The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology | date = 2018 | vauthors = Martinez Hernandez A, Urbanke H, Gillman AL, Lee J, Ryazanov S, Agbemenyah HY, Benito E, Jain G, Kaurani L, Grigorian G, Leonov A, Rezaei-Ghaleh N, Wilken P, Arce FT, Wagner J, Fuhrman M, Caruana M, Camilleri A, Vassallo N, Zweckstetter M, Benz R, Giese A, Schneider A, Korte M, Lal R, Griesinger C, Eichele G, Fischer A | journal = EMBO Molecular Medicine | volume = 10 | issue = 1 | pages = 32–47 | pmid = 29208638 | pmc = 5760857 }}</ref> which is associated with AD.


It is currently in clinical trials for Parkinson's disease and ].<ref>{{cite web | url = https://adisinsight.springer.com/drugs/800046788 | title = Emrusolmin - Modag | work = AdisInsight | publisher = Springer Nature Switzerland AG }}</ref> It is currently in clinical trials for Parkinson's disease and ].<ref>{{cite web | url = https://adisinsight.springer.com/drugs/800046788 | title = Emrusolmin - Modag | work = AdisInsight | publisher = Springer Nature Switzerland AG }}</ref>

Latest revision as of 07:58, 26 December 2024

Pharmaceutical compound
Emrusolmin
Clinical data
Other namesAnle138b, TEV-56286
Legal status
Legal status
  • Investigational
Identifiers
IUPAC name
  • 5-(1,3-benzodioxol-5-yl)-3-(3-bromophenyl)-1H-pyrazole
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
Chemical and physical data
FormulaC16H11BrN2O2
Molar mass343.180 g·mol
3D model (JSmol)
SMILES
  • C1OC2=C(O1)C=C(C=C2)C3=CC(=NN3)C4=CC(=CC=C4)Br
InChI
  • InChI=InChI=1S/C16H11BrN2O2/c17-12-3-1-2-10(6-12)13-8-14(19-18-13)11-4-5-15-16(7-11)21-9-20-15/h1-8H,9H2,(H,18,19)
  • Key:RCQIIBJSUWYYFU-UHFFFAOYSA-N

Emrusolmin (development code Anle138b) is an experimental drug for the treatment of neurodegenerative diseases. It is an inhibitor of protein aggregation, particularly preventing the aggregation of α-synuclein which is implicated in the development of Parkinson's disease. Other proteins it inhibits the aggregation of include tau which is associated with Alzheimer's disease (AD) and tauopathy, and amyloid beta which is associated with AD.

It is currently in clinical trials for Parkinson's disease and multiple system atrophy.

References

  1. Wagner J, Ryazanov S, Leonov A, Levin J, Shi S, Schmidt F, et al. (2013). "Anle138b: A novel oligomer modulator for disease-modifying therapy of neurodegenerative diseases such as prion and Parkinson's disease". Acta Neuropathologica. 125 (6): 795–813. doi:10.1007/s00401-013-1114-9. PMC 3661926. PMID 23604588.
  2. Dervişoğlu R, Antonschmidt L, Nimerovsky E, Sant V, Kim M, Ryazanov S, et al. (2023). "Anle138b interaction in α-synuclein aggregates by dynamic nuclear polarization NMR". Methods. 214: 18–27. doi:10.1016/j.ymeth.2023.04.002. PMID 37037308.
  3. Antonschmidt L, Matthes D, DervişOğLu R, Frieg B, Dienemann C, Leonov A, et al. (2022). "The clinical drug candidate anle138b binds in a cavity of lipidic α-synuclein fibrils". Nature Communications. 13 (1): 5385. Bibcode:2022NatCo..13.5385A. doi:10.1038/s41467-022-32797-w. PMC 9474542. PMID 36104315.
  4. Wagner J, Krauss S, Shi S, Ryazanov S, Steffen J, Miklitz C, et al. (2015). "Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies". Acta Neuropathologica. 130 (5): 619–631. doi:10.1007/s00401-015-1483-3. PMC 4612332. PMID 26439832.
  5. Martinez Hernandez A, Urbanke H, Gillman AL, Lee J, Ryazanov S, Agbemenyah HY, et al. (2018). "The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology". EMBO Molecular Medicine. 10 (1): 32–47. doi:10.15252/emmm.201707825. PMC 5760857. PMID 29208638.
  6. "Emrusolmin - Modag". AdisInsight. Springer Nature Switzerland AG.
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