Amlenetug

Amlenetug (Lu-AF82422) (2 μg/mL) binds human, cynomolgus monkey, rat, and mouse α-syn with Octet response values of 2.9-3.5 nm, while showing no detectable binding to human β-syn or γ-syn^[1].
Amlenetug (50 nM; RT 1 h-RT 30 min) binds MSA-derived α-syn aggregates with an EC₅₀ of 0.09 nM and binds PD-derived α-syn aggregates with an EC₅₀ of 0.16 nM^[1].
Amlenetug (50 nM; RT 1 h-RT 30 min) binds recombinant PFF-type fibrillar α-syn with an EC₅₀ of 0.30 nM^[1].
Amlenetug (1 µg/mL; 30 s) binds recombinant human monomeric α-syn via SPR with a K_D of 36 nM^[1].
Amlenetug binds α-syn oligomers with 0.3 nM affinity and monomers with 12 nM affinity via MDS^[1].
Amlenetug (1.25 μg/mL; 10-30 min) immunohistochemically labels pathological α-syn inclusions in human PD, DLB, and MSA brain tissue, including LBs, LNs, and GCIs^[1].
Amlenetug (8 μg antibody/mg magnetic beads; 120 min at 4°C-5 min at 95°C) immunoprecipitates full-length and truncated α-syn from human MSA, PD, and DLB brain homogenates, and enriches pS129 α-syn from MSA tissue^[1].
Amlenetug immunodepletes aggregated α-syn in MSA, PD, and DLB brain homogenates to control-sample levels^[1].
Amlenetug (7-fold dilution series; RT 15 min) inhibits α-syn aggregation induced by P91, Ribbons, Fibrils, PFF, MSA brain extracts, and truncated α-syn 1-119 seeds in F28 primary mouse neurons in a dose-dependent manner^[1].
Amlenetug (250 µg/mL; 15 min) prevents the accumulation of truncated 12 kDa α-syn seed species and inhibits the formation of insoluble aggregated α-syn in wild-type and F28 primary mouse neurons^[1].
Amlenetug (dilution series; 15 min) inhibits pHrodo-labeled PFF seed uptake in F28 primary mouse neurons by approximately 80% at the highest tested concentration^[1].
Amlenetug binds monomeric α-syn with a monovalent K_D of 16 nM by Biacore^[3].
Amlenetug (1 hour) binds α-syn PFF with an ELISA EC₅₀ of 0.05 nM^[3].
Amlenetug (1 μg/mL; 1 hour) exhibits strong selectivity for α-syn PFF over monomers in dot blot analysis^[3].
Amlenetug binds to α-syn PFF and co-localizes with it, as shown by TEM^[3].
Amlenetug (0.05-50 μg/mL) binds Lewy pathology, but in human Parkinson's disease brain tissue it also shows non-Lewy reactivity without selective Lewy staining^[3].
Amlenetug (1-10 µg/mL; 24 hours) inhibits α-syn PFF uptake in rat cortical neurons, with an inhibition rate of 89% at 1 µg/mL^[3].
Amlenetug (5-15 µg/mL; 13 days) reduces PFF seed-formed pS129 α-syn in rat cortical neurons, with an inhibition rate of 78% at 5 µg/mL^[3].
Amlenetug (10-100 µg/mL; 6 days) inhibits α-syn PFF-induced aggregation in HEK293 FRET reporter cells, with an inhibition rate of 54% at 10 µg/mL^[3].

Amlenetug (10-3,000 µg/mL; 20 minutes) does not alter the phagocytic capacity of human whole blood monocytes^[4].

Amlenetug (up to 1,000 µg/mL; 30 minutes) does not activate human monocytes and does not alter IFNα, IL-6, or LPS-induced monocyte activation^[4].

Amlenetug (5-350 µg/mL) does not bind to human erythrocytes or resting/TRAP6-activated platelets, and binds only a low proportion (0-15%) of human monocytes in an Fc-independent manner^[4].
Amlenetug (0.064-10,000 µg/mL; 24-48 hours) does not induce cytokine release from human whole blood or PBMCs across the tested concentration range^[4].
Amlenetug (0.5-2 µg/mL) specifically binds to human neural tissues in tissue sections, including the cerebellum, cerebral cortex, colonic myenteric plexus, eye, ileal myenteric plexus, pars nervosa of the pituitary, peripheral nerves, and spinal cord, and the staining intensity generally increases as the concentration rises from 0.5 to 2 µg/mL^[4].