**Background:** Armeniacae semen amarum (ASA), also known as Kuxingren or bitter apricot seed, is a traditional Chinese herbal drug derived from seeds of Prunus armeniaca L. and related Rosaceae species. It has a long history of use for treating cough, asthma, and constipation. Despite extensive research, a comprehensive review of its botany, phytochemistry, pharmacology, clinical applications, toxicology, and pharmacokinetics was lacking. This review aims to systematically summarize these aspects to facilitate further research and clinical application.
**Methods:** The authors conducted a comprehensive literature search using PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), and Google Scholar, with keywords including ASA, its bioactive components, and ASA-containing formulas, up to December 2023. They compiled and analyzed data on botanical features, traditional uses, phytochemical components, pharmacological activities, clinical applications, toxicological effects, and pharmacokinetic profiles.
**Key Results:** The review identified 170 chemical components from ASA, categorized into glycosides (including amygdalin, neoamygdalin, prunasin), organic acids (39 compounds, including fatty acids like oleic and linoleic acid), amino acids (18, including 8 essential), flavonoids (43, including catechin, epicatechin, quercetin derivatives), terpenoids (20), phytosterols (10), phenylpropanoids (16), and other compounds. Pharmacological activities were extensive: anticancer activity was demonstrated in breast carcinoma (e.g., IC50 for MCF-7 cells: 200.6 μg/mL at 24 h), prostatic cancer, hepatocellular carcinoma, lung cancer, renal cell carcinoma, bladder cancer, and others, primarily through inhibition of cell adhesion, migration, proliferation, and induction of apoptosis via pathways involving integrins, Bcl-2/Bax, caspase-3, and NF-κB. Anti-oxidant activity was shown via scavenging DPPH radicals (IC50 = 3.05 mg/mL for polyphenols) and increasing SOD and GSH levels. Antimicrobial activity was observed against Gram-positive and Gram-negative bacteria (e.g., MIC = 250-500 μg/mL for volatile oil against S. aureus and E. coli) and fungi. Anti-inflammatory effects were mediated through inhibition of TGF-β1/Smad and TLR4/NF-κB pathways. Cardiovascular protection included reducing LDL-C by 21.2% after 12 weeks of 60 mg/kg ASA in a clinical study. Neuroprotection, respiratory protection (including against COVID-19 targets), digestive system protection, antidiabetic effects, and liver/kidney protection were also reported. Toxicologically, the LD50 of lyophilized ASA aqueous extract in mice was 29.9 g/kg, while amygdalin's LD50 was 880 mg/kg. Detoxification methods include processing with Ephedra herba or soaking in 25% sodium chloride solution. Pharmacokinetically, after oral administration of ASA water extract, amygdalin reached Cmax of 223.6 ng/mL at Tmax 0.5 h, while its metabolite prunasin reached Cmax of 5,212.8 ng/mL at Tmax 0.58 h, with bioavailability of amygdalin only 0.19% ± 0.08%.
**Clinical Implications:** ASA shows promise as a multi-target therapeutic agent for respiratory diseases, cancers, cardiovascular conditions, and inflammatory disorders. Its clinical use in traditional Chinese medicine is supported by numerous formulas in the Chinese Pharmacopoeia. However, its toxicity due to cyanide release necessitates careful processing and dosing. The low oral bioavailability of amygdalin and the need for more in vivo and clinical studies limit its immediate translation. Future research should focus on efficient detoxification methods, pharmacokinetics of other active compounds, and clinical trials to validate efficacy and safety.