Genetic, physiological, and biochemical data indicate that agglomerates of the 42-amino acid form of the amyloid-b (Ab42) peptide are strongly linked to Alzheimer’s disease (AD) etiology and thus represent a particularly attractive target for the development of an effective diseasemodifying approach for AD treatment. A plethora of chemical entities able to modulate Ab42 self-assembly have been developed in recent years, among them, several are in clinical or preclinical development.
Federica Belluti, Angela Rampa, Silvia Gobbi, Alessandra Bisi (2013). Small-molecule inhibitors/modulators of amyloid-β peptide aggregation and toxicity for the treatment of Alzheimer's disease: a patent review (2010 – 2012). EXPERT OPINION ON THERAPEUTIC PATENTS, 23, 581-596 [10.1517/13543776.2013.772983].
Small-molecule inhibitors/modulators of amyloid-β peptide aggregation and toxicity for the treatment of Alzheimer's disease: a patent review (2010 – 2012)
BELLUTI, FEDERICA;RAMPA, ANGELA;GOBBI, SILVIA;BISI, ALESSANDRA
2013
Abstract
Genetic, physiological, and biochemical data indicate that agglomerates of the 42-amino acid form of the amyloid-b (Ab42) peptide are strongly linked to Alzheimer’s disease (AD) etiology and thus represent a particularly attractive target for the development of an effective diseasemodifying approach for AD treatment. A plethora of chemical entities able to modulate Ab42 self-assembly have been developed in recent years, among them, several are in clinical or preclinical development.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.