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Monoclonal antibody
Type Whole antibody
Source Humanized
Target Beta amyloid
Clinical data
Legal status
  • Investigational
CAS Number 955085-14-0 N
ATC code None
ChemSpider none
UNII 5D6PWO0333 YesY
KEGG D10058 N
Chemical data
Formula C6396H9922N1712O1996S42
Molar mass 144.1 kDa
 NYesY (what is this?)  (verify)

Solanezumab (proposed INN) is a monoclonal antibody being investigated by Eli Lilly as a neuroprotector[1] for patients with Alzheimer's disease.[2][3] The drug attracted extensive media coverage proclaiming it as a supposed "breakthrough" although in reality the medical evidence in support of such claims is lacking.[4]

Solanezumab, or sola, binds the amyloid-β peptides that aggregate and form plaques in the brain that are an early pathological feature of Alzheimer's disease.[5] Sola binds the central epitope of monomeric amyloid-β, KLVFFAD, (PDB ID 4XXD[6]) with picomolar affinity.[7] This epitope is known as the nucleation site for Aβ oligomerization, and it is these oligomers of Aβ that are thought to be toxic to neurons.

The two Phase III trials were EXPEDITION 1 and EXPEDITION 2. EXPEDITION 1 didn't meet the predefined assessments. Lilly changed the predefined study goal in EXPEDITION 2, but EXPEDITION 2 didn't meet that goal either.[8][9]

An ex-FDA official told the Financial Times that solanezumab "does not have a snowball’s chance in a very hot place" of getting conditional approval. To the FDA, missing the primary endpoint in a Phase III trial is "fatal."[9]


  1. ^ International Nonproprietary Names for Pharmaceutical Substances (INN, prepublication copy), World Health Organization.
  2. ^ Clinical trial number NCT00749216 for "Solanezumab Safety Study in Japanese Patients With Alzheimer's Disease" at
  3. ^ Clinical trial number NCT00905372 for "Effect of LY2062430 on the Progression of Alzheimer's Disease (EXPEDITION)" at
  4. ^ McCartney M (2015). "Margaret McCartney: The "breakthrough" drug that's not been shown to help in Alzheimer's disease". BMJ 351: h4064. doi:10.1136/bmj.h4064. PMID 26208710. 
  5. ^ Villemagne, Victor L; Burnham, Samantha; Bourgeat, Pierrick; Brown, Belinda; Ellis, Kathryn A; Salvado, Olivier; Szoeke, Cassandra; MacAulay, S Lance; Martins, Ralph; Maruff, Paul; Ames, David; Rowe, Christopher C; Masters, Colin L; Australian Imaging Biomarkers Lifestyle (AIBL) Research Group (2013). "Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: A prospective cohort study". The Lancet Neurology 12 (4): 357–67. doi:10.1016/S1474-4422(13)70044-9. PMID 23477989. 
  6. ^ Crespi, Gabriela A. N.; Hermans, Stefan J.; Parker, Michael W.; Miles, Luke A. (2015). "Molecular basis for mid-region amyloid-β capture by leading Alzheimer's disease immunotherapies". Scientific Reports 5: 9649. doi:10.1038/srep09649. PMID 25880481. 
  7. ^ Watt, Andrew D.; Crespi, Gabriela A. N.; Down, Russell A.; Ascher, David B.; Gunn, Adam; Perez, Keyla A.; McLean, Catriona A.; Villemagne, Victor L.; Parker, Michael W.; Barnham, Kevin J.; Miles, Luke A. (2014). "Do current therapeutic anti-Aβ antibodies for Alzheimer's disease engage the target?". Acta Neuropathologica 127 (6): 803–10. doi:10.1007/s00401-014-1290-2. PMID 24803227. 
  8. ^ Christian Nordvist (9 Oct 2012). "Lilly's Solanezumab Slows Down Alzheimer's Progression". Medical News Today. 
  9. ^ a b Anusha Kambhampathy, Jenifer C. Smith-Parker. (4 Sep 2012). "Eli Lilly’s solanezumab faces grim prospects of attaining conditional FDA approval in mild Alzheimer’s". Financial Times.