Hermetica Superfood Encyclopedia
Carthamin is a red chalcone pigment derived from safflower (Carthamus tinctorius) that exerts its biological effects primarily through antioxidant activity, inhibition of platelet aggregation, and modulation of inflammatory signaling pathways. It has been investigated in preclinical models for cardiovascular protection, kidney preservation, and anticoagulant properties.


Carthamin is a bioactive red-yellow pigment extracted from the florets of Carthamus tinctorius L. (safflower), belonging to the chalcone glucoside family. It is produced through enzymatic conversion from precursor compounds like precarthamin, with extraction typically involving macroporous resin adsorption from safflower petals followed by purification.
Current evidence for carthamin is limited to preclinical animal and in vitro studies, with no human clinical trials identified. Key studies include a rat diabetic nephropathy model showing reduced renal fibrosis with 65 mg/kg carthamin yellow liposomes (PMID:39904762), and a rat blood stasis model demonstrating improved hemorheological parameters (PMID:19406191).

No clinically studied human dosages are available. Animal studies used 65 mg/kg intraperitoneally in rats for 4 weeks, with liposomal formulations showing enhanced bioavailability compared to free carthamin. Consult a healthcare provider before starting any new supplement.
Carthamin (C43H42O22, MW ~910.8 g/mol) is a red chalcone-type pigment and the principal water-insoluble flavonoid pigment of safflower (Carthamus tinctorius L.) florets. It is not a nutritional macronutrient source but rather a bioactive compound consumed in trace quantities, primarily through safflower flower tea (hong hua tea) or as a component of safflower-derived food colorants. Key biochemical details: • Classification: Chalcone glycoside (C-glucosylquinochalcone); formed by oxidation of the yellow precursor precarthamin (hydroxysafflor yellow A pathway-related) during flower maturation. • Typical concentration in safflower florets: approximately 0.3–0.6% of dry petal weight, though this varies significantly by cultivar, harvest stage, and drying method. • In traditional safflower flower tea preparations (1–3 g dried florets per serving), carthamin intake is estimated at roughly 3–18 mg per cup, though most carthamin is poorly water-soluble and remains largely in the petal residue; hot water extraction yields are low (<10–15% of total carthamin content). • Bioactive co-constituents in safflower florets that accompany carthamin include hydroxysafflor yellow A (HSYA, ~1–2% of dry weight), kaempferol glycosides, quercetin derivatives, luteolin, and safflor yellow B. • Carthamin itself contains no significant vitamins, minerals, protein, fat, or dietary fiber — it is consumed for its pharmacological/bioactive properties rather than macronutrient value. • Bioavailability: Oral bioavailability is considered low due to poor aqueous solubility, high molecular weight, and extensive glycosylation. Preliminary pharmacokinetic data (animal models) suggest limited intestinal absorption; gut microbiota-mediated deglycosylation may produce smaller aglycone metabolites with potentially improved absorption, but human pharmacokinetic data are essentially absent. • Key functional groups contributing to bioactivity: quinochalcone core with multiple phenolic hydroxyl groups conferring antioxidant capacity (ORAC and DPPH radical scavenging activity documented in vitro), carbonyl groups, and glucose moieties. • Antioxidant potency: In vitro IC50 values for DPPH radical scavenging have been reported in the range of ~15–50 µM depending on assay conditions, comparable to but generally lower than pure quercetin or HSYA. • No established Recommended Daily Intake, Adequate Intake, or Upper Tolerable Limit exists for carthamin. Traditional Chinese Medicine dosing of safflower flowers (containing carthamin) is typically 3–10 g dried florets per day in decoction form.
Carthamin scavenges reactive oxygen species (ROS) and suppresses NF-κB-mediated inflammatory signaling, reducing downstream cytokine production including TNF-α and IL-6. In renal tissue, it inhibits TGF-β1-driven fibrotic pathways, decreasing collagen deposition and reducing proteinuria in diabetic nephropathy models. Its antiplatelet effect is mediated through inhibition of thromboxane A2 synthesis and interference with ADP-induced platelet aggregation cascades.
Research on carthamin remains largely confined to in vitro cell studies and rodent animal models, with no robust human clinical trials published to date. In rat models of diabetic nephropathy, carthamin administration reduced urinary protein excretion and renal fibrosis markers including α-SMA and fibronectin. Myocardial ischemia/reperfusion injury studies in rodents demonstrated reductions in creatine kinase (CK) and lactate dehydrogenase (LDH) leakage, indicating reduced cardiomyocyte damage. The evidence is preliminary and cannot be extrapolated to human dosing or efficacy without controlled clinical trials.
Carthamin has not been evaluated for safety in formal human clinical trials, so a comprehensive side effect profile is not established. Due to its antiplatelet and potential anticoagulant activity, it may theoretically potentiate the effects of blood-thinning medications such as warfarin, aspirin, clopidogrel, or NSAIDs, increasing bleeding risk. Safflower-derived compounds including carthamin are generally contraindicated in pregnancy due to potential uterine-stimulating effects historically associated with the plant. Individuals with bleeding disorders or those scheduled for surgery should avoid carthamin-containing products until more safety data are available.