Chlorogenic acid is a derivative of caffeic acid and quinic acid; it has an antioxidant activity. Chlorogenic acid has been combined with gadolinium to develop a therapeutic and diagnostic nanodelivery system for MRI imaging. In a rat model of diabetes mellitus, chlorogenic acid counteracted the alterations in lipid profiles typical of type-2 diabetes, especially when administered in combination with tetrahydrocurcumin. In mice fed with a high-fat diet, the consumption of chlorogenic acid resulted in an anti-obesity action that lowered the blood levels of cholesterol and triglycerides. In humans, it is readily absorbed in the intestinal tract.

Chlorogenic acid is a phenolic natural product isolated from the leaves and fruits of dicotyledonous plants, including the coffee bean. Structurally, chlorogenic acid is the ester of caffeic acid with the 3-hydroxyl group of quinic acid. Chlorogenic acid is an important factor in plant metabolism. It is also an antioxidant and an inhibitor of the tumor promoting activity of phorbol esters.Chlorogenic acid, at concentrations as high as 100 µM, does not inhibit the 5-lipoxygenase activity of ionophore-stimulated human polymorphonuclear leukocytes.

It has broad antibacterial effect, advantageous bravery, hemostatic, increase white blood cell and antiviral effect, the effect of the blood clotting and bleeding time is shortened. It is used in the treatment of upper respiratory tract infection, anti-inflammatory and antipyretic, cool blood heat dissipation. Used as pharmaceutical raw materials and intermediates. clearing heat and removing toxicity, cold wind heat, broad-spectrum antimicrobial properties, having obvious inhibitory effect to hemolytic streptococcus, dysentery rod gas and salmonella typhi bacteria

Chlorogenic Acid is an analog of caffeic acid (sc-200499) that displays antioxidant, analgesic, antipyretic and chemopreventive activity. Chlorogenic acid inhibits Bcr-Abl (the fusion protein of Bcr and c-Abl) tyrosine kinase and triggers MAP kinases p38-dependent apoptosis. Chlorogenic acid has been documented to inhibit growth of A549 human cancer cells in vitro. In a dose dependent manner chlorogenic acid suppressed 12-O-tetradecanoylphorbol-13- acetate (TPA)-induced neoplastic transformation of JB6 P+ cells. When JB6 P+ cells were pretreated with chlorogenic acid, UVB- or TPA-induced transactivation of AP-1 and NF-κ B were blocked and at lower doses, chlorogenic acid decreased the phosphorylation of c-Jun NH2-terminal kinases, MAPK kinase 4, and p38 kinase. In the same study, chlorogenic acid also increased the activities of GST and NAD(P)H. In IL-1 induced HUVEC cells Chlorogenic acid dose-dependently suppressed IL-1 beta-induced mRNA expression of endothelial cell selectin, VCAM-1, and ICAM-1, production of ROS, and attenuated or blocked IL-1 beta-induced nuclear translocation of NF-κ B subunits p50 and p65, which in turn transcriptionally attenuated CAM. In addition to all of these actions, chlorogenic acid, in a dose-response manner, was observed to markedly reduce the adhesion of human monocyte cells to IL-1 β-treated HUVEC cells. The compound has also been observed to inhibit in vitro DNA methylation.