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| Rauwolfia serpentina - Indian Snakeroot, Sarpagandha Type: Botanical extract / indole alkaloid-containing medicinal plant Active Constituents: Reserpine, ajmaline, ajmalicine, serpentine, rescinnamine, and related indole alkaloids. Function: Rauwolfia serpentina contains pharmacologically active indole alkaloids with effects on monoamine transport, adrenergic signaling, cardiovascular regulation, cell proliferation, apoptosis, and other signaling pathways. Cancer: Experimental evidence suggests anticancer activity for Rauwolfia-derived alkaloids, particularly reserpine, including inhibition of proliferation, induction of apoptosis, and cell-cycle disruption. Evidence for whole Rauwolfia serpentina extract is more limited than for isolated constituents or other Rauwolfia species, so species-specific attribution should be maintained. Rauwolfia serpentina — also called Indian snakeroot or Sarpagandha, is a medicinal plant in the Apocynaceae family whose roots contain pharmacologically active monoterpenoid indole alkaloids, most notably reserpine, along with ajmaline, ajmalicine, serpentine, rescinnamine, and related compounds. It is classified as a botanical medicinal product / indole-alkaloid source; Reserpine is the best-characterized constituent and acts primarily as an essentially irreversible vesicular monoamine transporter inhibitor, especially VMAT2, depleting norepinephrine, dopamine, and serotonin from neuronal and sympathetic storage vesicles. Historically, Rauwolfia preparations and reserpine were used as antihypertensive agents. Cancer evidence is substantially stronger for isolated reserpine than for standardized R. serpentina extracts, and results from other Rauvolfia species should not automatically be attributed to R. serpentina. Primary mechanisms (ranked):
Bioavailability / PK relevance: Reserpine is orally absorbed, widely distributed, crosses the blood-brain barrier and placenta, and accumulates substantially in tissues including adipose tissue. Human pharmacokinetic data indicate biphasic elimination, with an early half-life of approximately 4.5 hours and a terminal phase of approximately 11.3 days; pharmacodynamic effects can therefore persist well beyond plasma exposure. Whole-root preparations have variable alkaloid composition and cannot be assumed pharmacokinetically equivalent to purified reserpine. In-vitro vs systemic exposure relevance: Anticancer findings are predominantly from cell-culture or animal experiments using purified reserpine or extracts whose achievable human tumor exposure is uncertain. Concentrations producing cancer-cell effects should therefore not be assumed achievable or safe with oral R. serpentina. Chronic pharmacological effects may occur at low systemic reserpine exposure because VMAT binding and monoamine depletion are prolonged, but this does not establish clinically relevant anticancer exposure. Clinical evidence status: Hypertension: historical controlled human evidence and established pharmacology. Cancer: preclinical only; no established anticancer clinical efficacy. Human studies of Rauwolfia/reserpine primarily concern hypertension rather than cancer. Major constraints include hypotension, bradycardia, CNS monoamine depletion, depression, Parkinsonian/extrapyramidal effects, gastrointestinal hypersecretion, drug interactions, and prolonged pharmacodynamic action. Reserpine-containing labeling also notes animal tumorigenicity and uncertain historical epidemiologic findings concerning breast cancer, making indiscriminate interpretation of reserpine as an anticancer compound inappropriate. Rauwolfia serpentina Cancer-Relevant Mechanisms
P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| Also called CCND1 Gatekeeper of Cell-Cycle Commitment The main function of cyclin D1 is to maintain cell cycle and to promote cell proliferation. Cyclin D1 is a key regulatory protein involved in the cell cycle, particularly in the transition from the G1 phase to the S phase. It is part of the cyclin-dependent kinase (CDK) complex, where it binds to CDK4 or CDK6 to promote cell cycle progression. Cyclin D1 is crucial for the regulation of the cell cycle. Overexpression or dysregulation of cyclin D1 can lead to uncontrolled cell proliferation, a hallmark of cancer. Cyclin D1 is often found to be overexpressed in various cancers. Cyclin D1 can interact with tumor suppressor proteins, such as retinoblastoma (Rb). When cyclin D1 is overexpressed, it can lead to the phosphorylation and inactivation of Rb, releasing E2F transcription factors that promote the expression of genes required for DNA synthesis and cell cycle progression. Cyclin D1 is influenced by various signaling pathways, including the PI3K/Akt and MAPK pathways, which are often activated in cancer. In some cancers, high levels of cyclin D1 expression have been associated with poor prognosis, making it a potential biomarker for cancer progression and treatment response. |
| 7378- | RS, | Reserpine inhibits DNA repair, cell proliferation, invasion and induces apoptosis in oral carcinogenesis via modulation of TGF-β signaling |
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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