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| Capsaicin is a chemical compound that gives chili peppers their spicy flavor and heat. Biological activity, capsaicin has been reported to exhibit a range of effects, including: Pain relief: 10-50 μM Anti-inflammatory activity: 20-50 μM Antioxidant activity: 10-100 μM Anti-cancer activity: 50-100 μM Cardiovascular health: 20-50 μM Approximate μM concentrations of capsaicin, the active compound in chili peppers, that can be achieved with different amounts of chili peppers: 1 teaspoon of dried chili pepper flakes (5g):~10-50 μM of capsaicin 1 tablespoon of dried chili pepper flakes (15g): ~30-150 μM of capsaicin 1 cup of fresh chili peppers (100g): ~100-500 μM of capsaicin 1 teaspoon of chili pepper extract (5g): ~100-500 μM of capsaicin 1 tablespoon of chili pepper extract (15g): ~300-1500 μM of capsaicin Approximate μM concentrations of capsaicin in various foods that contain capsaicin: Jalapeño peppers: 1 pepper (20g): ~20-100 μM of capsaicin 2–8 mg/100g of fresh Jalapeño Serrano peppers: 1 pepper (10g): ~10-50 μM of capsaicin 5–15 mg/100g Cayenne peppers: 1 pepper (10g): ~50-200 μM of capsaicin Habanero peppers: 1 pepper (20g): ~100-500 μM of capsaicin 15–30 mg/100g Ghost peppers: 1 pepper (20g): ~200-1000 μM of capsaicin Hot sauce: 1 teaspoon (5g): ~10-50 μM of capsaicin Chili flakes: 1 teaspoon (5g): ~10-50 μM of capsaicin Spicy sauces and marinades: 1 tablespoon (15g): ~10-50 μM of capsaicin Cayenne Pepper Powder – Approximate capsaicin content: roughly 5–20 mg/g (15-30g human for 100uM?) -IC50 in Cancer Cell Lines: Approximately 50–300 µM (consume 150mg of capsaican not possible?) -IC50 in Normal Cell Lines: Generally higher—often 2–3 times greater Pathways: -disrupting mitochondrial membrane potential, leading to cytochrome c release and subsequent activation of caspases -Activation of TRPV1: resulting in increased intracellular calcium levels -capsaicin can lead to increased production of ROS within cancer cells -Inhibition of NF-κB -Inhibit PI3K/AKT/mTOR signaling -STAT3 Inhibition -Cell Cycle Arrest -reduce the expression of vascular endothelial growth factor (VEGF) -COX-2 -capsaicin is a natural ADAM10 activator and shows potential to attenuate amyloid pathology and protect against AD Capsaicin — capsaicin is a pungent vanilloid alkaloid phytochemical from Capsicum peppers and the principal TRPV1 agonist responsible for chili heat. It is best classified as a natural product / small-molecule vanilloid with approved topical analgesic use but no established anticancer indication. Standard abbreviations include CAP and CAPS. In cancer literature it is a pleiotropic stressor whose dominant preclinical effects usually converge on Ca2+ influx, mitochondrial dysfunction, ROS generation, suppression of pro-survival signaling, and apoptosis, but its biology is context- and concentration-dependent, with occasional low-dose pro-migratory / pro-metastatic signaling reported. Primary mechanisms (ranked):
Bioavailability / PK relevance: Capsaicin is lipophilic, rapidly absorbed, and rapidly metabolized, with substantial first-pass limitation after oral exposure. Human oral PK from a capsicum preparation containing 26.6 mg capsaicin produced a Cmax of about 2.47 ng/mL at ~47 minutes, while the FDA-approved 8% topical system produced transient systemic exposure usually below 5 ng/mL, with a highest detected plasma level of 4.6 ng/mL. Delivery is therefore a major translation constraint for anticancer use, and formulation-based approaches are often invoked to overcome short half-life, irritancy, and exposure limits. In-vitro vs systemic exposure relevance: This is a major limitation. Many anticancer cell studies use roughly 10–300 µM, whereas reported human plasma exposures from oral or approved topical use are in the low ng/mL range, approximately ~0.008–0.015 µM, i.e., orders of magnitude lower than many cytotoxic in-vitro concentrations. Accordingly, direct systemic tumoricidal translation from standard dietary or approved topical exposure is weak unless local delivery, sustained-release systems, or substantially altered formulations are used. Clinical evidence status: Anticancer evidence is predominantly preclinical, with in-vitro and some in-vivo support across several tumor types. There is no regulatory approval for cancer treatment. Human oncology use is currently much more credible as supportive care for neuropathic pain, especially chemotherapy-induced peripheral neuropathy, where topical high-concentration capsaicin patches are being studied and used off-label / investigationally, rather than as a direct antitumor therapy. Mechanistic Table
P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| Tumor cell invasion is a critical process in cancer progression and metastasis, where cancer cells spread from the primary tumor to surrounding tissues and distant organs. This process involves several key steps and mechanisms: 1.Epithelial-Mesenchymal Transition (EMT): Many tumors originate from epithelial cells, which are typically organized in layers. During EMT, these cells lose their epithelial characteristics (such as cell-cell adhesion) and gain mesenchymal traits (such as increased motility). This transition is crucial for invasion. 2.Degradation of Extracellular Matrix (ECM): Tumor cells secrete enzymes, such as matrix metalloproteinases (MMPs), that degrade the ECM, allowing cancer cells to invade surrounding tissues. This degradation facilitates the movement of cancer cells through the tissue. 3.Cell Migration: Once the ECM is degraded, cancer cells can migrate. They often use various mechanisms, including amoeboid movement and mesenchymal migration, to move through the tissue. This migration is influenced by various signaling pathways and the tumor microenvironment. 4.Angiogenesis: As tumors grow, they require a blood supply to provide nutrients and oxygen. Tumor cells can stimulate the formation of new blood vessels (angiogenesis) through the release of growth factors like vascular endothelial growth factor (VEGF). This not only supports tumor growth but also provides a route for cancer cells to enter the bloodstream. 5.Invasion into Blood Vessels (Intravasation): Cancer cells can invade nearby blood vessels, allowing them to enter the circulatory system. This step is crucial for metastasis, as it enables cancer cells to travel to distant sites in the body. 6.Survival in Circulation: Once in the bloodstream, cancer cells must survive the immune response and the shear stress of blood flow. They can form clusters with platelets or other cells to evade detection. 7.Extravasation and Colonization: After traveling through the bloodstream, cancer cells can exit the circulation (extravasation) and invade new tissues. They may then establish secondary tumors (metastases) in distant organs. 8.Tumor Microenvironment: The surrounding microenvironment plays a significant role in tumor invasion. Factors such as immune cells, fibroblasts, and signaling molecules can either promote or inhibit invasion and metastasis. |
| 5844- | CAP, | Non-pungent long chain capsaicin-analogs arvanil and olvanil display better anti-invasive activity than capsaicin in human small cell lung cancers |
| - | in-vitro, | Lung, | DMS114 |
| 1263- | CAP, | Capsaicin inhibits the migration and invasion via the AMPK/NF-κB signaling pathway in esophagus sequamous cell carcinoma by decreasing matrix metalloproteinase-9 expression |
| - | in-vitro, | ESCC, | Eca109 |
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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