After ingestion of amygdalin, β-glucosidase enzymes in the digestive system metabolize amygdalin producing hydrogen cyanide and this hydrogen cyanide produced will find its way to tumor cells which is thought to have a potent cytotoxic effect. thus destroying them. It has been considered to be hydrolyzed only in cancer cells

Several experiments have shown induction of apoptosis by amygdalin as a result of increased expression of Bax protein and caspase-3 and reduced expression of antiapoptotic BcL-2protein. Amygdalin has also been shown to inhibit the adhesion of breast cancer cells, lung cancer cells and bladder cancer cells by decreased expression of integrin's, reduction of catenin levels and inhibition of the Akt-mTOR pathway, which may consequently lead to inhibition of metastases of cancer cells. It has also been revealed that amygdalin in renal cancer cells increased expression of p19 protein resulting in inhibition of cell transfer from G1-phase to S-phase, and thus inhibited cell proliferation. Other studies have indicated that amygdalin inhibits NF-kβ and NLRP3 signaling pathways, and consequently has anti-inflammatory effect due to reducing the expression of proinflammatory cytokines such as pro-IL-1β.

apoptosis is a central process activated by amygdalin in cancer cells. It is suggested to stimulate apoptotic process by upregulating expression of Bax (proapoptotic protein) and caspase-3 and downregulating expression of Bcl-2 (anti-apoptotic protein). It also promotes arrest of cell cycle in G0/G1 phase and decrease number of cells entering S and G2/M phases. Thus, it is proposed to enhance deceleration of cell cycle by blocking cell proliferation and growth.