| Features: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 |
| Source: CGL-CS |
| Type: |
| Mitogen-activated protein kinases (MAPKs) are a group of proteins involved in transmitting signals from the cell surface to the nucleus, playing a crucial role in various cellular processes, including growth, differentiation, and apoptosis (programmed cell death). MAPK Pathways: The MAPK family includes several pathways, the most notable being: 1.ERK (Extracellular signal-Regulated Kinase): Often associated with cell proliferation and survival. 2.JNK (c-Jun N-terminal Kinase): Typically involved in stress responses and apoptosis. 3.p38 MAPK: Associated with inflammatory responses and apoptosis. Inhibitors: Targeting the MAPK pathway has become a strategy in cancer therapy. For example, BRAF inhibitors (like vemurafenib) are used in treating melanoma with BRAF mutations. Altered Expression Levels: Overexpression: Many cancers exhibit overexpression of MAPK pathway components, such as RAS, BRAF, and MEK. This overexpression can lead to increased signaling activity, promoting cell proliferation and survival. Downregulation: In some cases, negative regulators of the MAPK pathway (e.g., MAPK phosphatases) may be downregulated, leading to enhanced MAPK signaling. The expression levels of MAPK pathway components can serve as biomarkers for cancer diagnosis, prognosis, and treatment response. For example, high levels of phosphorylated ERK (p-ERK) may indicate active MAPK signaling and poor prognosis in certain cancers. Numerous reports indicate that the MAPK pathway plays a major role in tumor progression and invasion, while inhibition of MAPK signaling reduces invasion. |
| 6625- | Cic, | Ech, | Chicoric acid supplementation prevents systemic inflammation-induced memory impairment and amyloidogenesis via inhibition of NF-κB |
| - | in-vivo, | NA, | NA |
| 6626- | Cic, | Ech, | Chicoric Acid Ameliorated Beta-Amyloid Pathology and Enhanced Expression of Synaptic-Function-Related Markers via L1CAM in Alzheimer’s Disease Models |
| - | in-vivo, | Nor, | 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#:181 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid