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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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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 6623- | Cic, | MTX, | Chicoric acid prevents methotrexate hepatotoxicity via attenuation of oxidative stress and inflammation and up-regulation of PPARγ and Nrf2/HO-1 signaling |
| - | in-vivo, | Nor, | NA |
| 6631- | Cic, | Chicoric acid is a potent anti-atherosclerotic ingredient by anti-oxidant action and anti-inflammation capacity. |
| - | in-vitro, | 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
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