Alzheimer’s disease (AD) is a neurodegenerative condition associated with the misfolding and aggregation of proteins. Pathologically, it is marked by the presence of senile plaques, which consist of extracellular amyloid-β (Aβ) peptides, and intracellular neurofibrillary tangles (NFTs), comprised of hyperphosphorylated tau proteins. Extensive synaptic loss and neuronal degeneration underlie the memory deficits, cognitive decline, and behavioral disturbances characteristic of AD. The accumulation of amyloid-β (Aβ) peptides is considered a fundamental neuropathological hallmark of the disease, with its dysregulation playing a crucial role in AD onset. Amyloid-β (Aβ) is generated through the processing of amyloid precursor protein (APP) by β- and γ-secretases, with α-secretase cleavage resulting in non-amyloidogenic products. According to the amyloid cascade hypothesis, dysregulation in Aβ levels leads to its accumulation and aggregation into soluble oligomers and insoluble fibrils. Soluble oligomers are synaptotoxic and can induce tau hyperphosphorylation, while insoluble fibrils form senile plaques, triggering proinflammatory responses and contributing to oxidative stress, neuronal degeneration, and neuroinflammation. Therapeutic strategies targeting Aβ proteins hold promise as a disease-modifying approach for treating and preventing AD. This chapter presents recent discoveries on Aβ-targeted AD medications, including β-secretase inhibitors, γ-secretase inhibitors and modulators, α-secretase activators, direct inhibitors of Aβ aggregation, and immunotherapy targeting Aβ, with a focus on those currently undergoing clinical trials. Several drugs targeting Aβ show promise for near-term approval, with the recent FDA approval of the monoclonal anti-Aβ oligomers antibody, aducanumab, sparking both hopes and controversies. Most therapeutic approaches have concentrated on altering amyloid precursor protein processing or employing active or passive immunotherapy. Fewer investigations have assessed drugs that impact Aβ misfolding, aggregation, or clearance. While targeting β- and γ-secretase has yielded undesired outcomes, the activation of α-secretase and immunotherapy against Aβ oligomers show some promise.