ACD856

ACD856
Clinical data
Other namesACD-856
Routes of
administration
Oral[1][2]
Drug classTropomyosin receptor kinase TrkA, TrkB, and TrkC positive allosteric modulator[1][3][2][4]
Pharmacokinetic data
Elimination half-life~19 hours[5]

ACD856, or ACD-856, is a tropomyosin receptor kinase TrkA, TrkB, and TrkC positive allosteric modulator which is under development for the treatment of Alzheimer's disease, depressive disorders, sleep disorders, and traumatic brain injuries.[1][3][2][5][6][4] It is taken by mouth.[1][2]

  1. ^ a b c d "ACD 856". AdisInsight. Springer Nature Switzerland AG. 17 May 2024. Retrieved 23 October 2024.
  2. ^ a b c d "ACD856". ALZFORUM. 19 December 2023. Retrieved 23 October 2024.
  3. ^ a b "Delving into the Latest Updates on ACD-856 with Synapse". Synapse. 12 October 2024. Retrieved 23 October 2024.
  4. ^ a b Dahlström M, Madjid N, Nordvall G, Halldin MM, Vazquez-Juarez E, Lindskog M, et al. (July 2021). "Identification of Novel Positive Allosteric Modulators of Neurotrophin Receptors for the Treatment of Cognitive Dysfunction". Cells. 10 (8): 1871. doi:10.3390/cells10081871. PMC 8391421. PMID 34440640.
  5. ^ a b Forsell P, Parrado Fernández C, Nilsson B, Sandin J, Nordvall G, Segerdahl M (July 2024). "Positive Allosteric Modulators of Trk Receptors for the Treatment of Alzheimer's Disease". Pharmaceuticals. 17 (8): 997. doi:10.3390/ph17080997. PMC 11357672. PMID 39204102.
  6. ^ Wang D, Lang ZC, Wei SN, Wang W, Zhang H (2 May 2024). "Targeting brain-derived neurotrophic factor in the treatment of neurodegenerative diseases: A review". Neuroprotection. 2 (2). Wiley: 67–78. doi:10.1002/nep3.43. ISSN 2770-7296. ACD856 is an innovative allosteric modulator that positively affects all Trk receptors, amplifying their kinase activity. Subsequently, it potentiates the effect of BDNF or nerve growth factor (NGF) on neuronal survival, function, and plasticity of synapses. The finished phase I study showed that ACD856 passed the blood‐brain barrier and induced dose‐dependent treatment‐related alterations in quantitative electroencephalogram parameters with good safety.141,142