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| Cichoric acid Cichoric acid / Chicoric acid — Cichoric acid is a naturally occurring dicaffeoyltartaric acid polyphenol, formally a hydroxycinnamic acid derivative composed of two caffeic acid units esterified to tartaric acid. It is best classified as a plant-derived phenolic acid / caffeic-acid derivative rather than a drug. Standard abbreviations include Cic, ChicA, and CA, although CA is ambiguous because it is also used for caffeic acid, chlorogenic acid, carnosic acid, and many other database entries. Major sources include Echinacea purpurea, chicory, lettuce, basil, dandelion, and other Asteraceae/Lamiaceae plants. It is commonly used as a quality-marker compound for Echinacea purpurea extracts, but its direct cancer-development status remains preclinical only. Primary mechanisms (ranked):
Bioavailability / PK relevance: Oral systemic translation is constrained by polyphenol-type absorption, metabolism, plasma protein binding, and formulation stability. Rat PK/tissue-distribution work exists, but direct human PK data for isolated cichoric acid are limited. Echinacea extract exposure cannot be assumed to equal isolated cichoric acid exposure because alkamides, polysaccharides, glycoproteins, caftaric acid, and other constituents may drive part of the immune effect. In-vitro vs systemic exposure relevance: Many mechanistic studies use low-to-high micromolar cichoric acid concentrations. These concentrations may exceed free systemic exposure achievable from ordinary oral Echinacea or food intake, especially after first-pass and microbial metabolism. Low-micromolar effects such as 5 μM otoprotection in zebrafish are more pharmacologically plausible than high-micromolar cytotoxicity screens, but human-equivalent exposure remains uncertain. Clinical evidence status: Cancer: preclinical only; no adequate human cancer trials for isolated cichoric acid. Immune / respiratory use: human evidence exists for Echinacea preparations, but not as isolated cichoric acid attribution. Alzheimer’s disease: preclinical only, with cell and animal-model support but no validated human clinical efficacy. Regulatory/deployment status: listed as a natural-health-product ingredient name by Health Canada; not an approved anticancer or AD therapeutic. Cichoric Acid Mechanistic Profile
TSF legend: P: 0–30 min R: 30 min–3 hr G: >3 hr Alzheimer’s disease relevance: Cichoric acid has meaningful AD-preclinical relevance but no validated human AD clinical evidence. The main AD rationale is neuroinflammation and amyloid-pathology modulation rather than direct symptomatic cholinergic therapy. In animal and cellular AD models, cichoric acid has been reported to reduce Aβ burden, lower APP/BACE1 markers, improve synaptic-function markers, and activate antioxidant signaling. This supports an AD database sub-entry as preclinical / experimental, not as a clinically established intervention. AD mechanisms (ranked):
Clinical evidence status: AD evidence remains preclinical. No adequate human RCT evidence supports cichoric acid as an Alzheimer’s disease treatment. Translation constraints include oral exposure, blood-brain exposure, dose standardization, and uncertainty over whether whole-plant extracts reproduce isolated cichoric acid effects. Cichoric Acid Alzheimer’s Disease Mechanistic Profile
TSF legend: P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| BACE stands for β-site APP-cleaving enzyme, also known as β-secretase. It plays a central role in the pathogenesis of Alzheimer’s disease by initiating the production of amyloid-β (Aβ) peptides, the primary components of amyloid plaques found in the brains of individuals with AD. -inhibiting BACE1 reduces Aβ production. BACE1 - Beta-Site APP Cleaving Enzyme 1 / β-Secretase 1 Abbreviation: BACE1, β-secretase, β-secretase 1 Type: Aspartyl protease / amyloidogenic APP-processing enzyme Function: BACE1 is a membrane-associated aspartyl protease that performs the initial β-secretase cleavage of amyloid precursor protein (APP). This cleavage generates soluble APPβ and the membrane-bound C99 fragment, which is subsequently cleaved by γ-secretase to produce amyloid-β peptides including Aβ40 and Aβ42. Alzheimer's Disease: ↑ Increased BACE1 expression or enzymatic activity promotes amyloidogenic APP processing and increases amyloid-β production. Elevated BACE1 activity has been reported in Alzheimer's disease and contributes to Aβ accumulation, plaque formation, synaptic dysfunction, and disease progression. BACE1 inhibition reduces Aβ production, although clinical BACE1 inhibitors have been limited by adverse effects related to the enzyme's normal physiological functions. |
| 6624- | Cic, | Chicoric acid supplementation ameliorates cognitive impairment induced by oxidative stress via promotion of antioxidant defense system |
| - | in-vivo, | AD, | NA | - | in-vivo, | Park, | NA |
| 6625- | Cic, | Ech, | Chicoric acid supplementation prevents systemic inflammation-induced memory impairment and amyloidogenesis via inhibition of NF-κB |
| - | in-vivo, | NA, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:416 Target#:1349 State#:% Dir#:1
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