DTS(dibenzyl trisulphide) from Anamu / TumCI Cancer Research Results

Anamu, DTS(dibenzyl trisulphide) from Anamu: Click to Expand ⟱
Features:
Anamu (Guinea Hen Weed) Anamu (Petiveria alliacea)
A herb that is indigenous to the Amazon rainforest and the tropical areas of the Caribbean, Central and South America and Africa.
Anamu has been used for a wide variety of conditions, including arthritis, digestive disorders, infections, diabetes, cancer, for pain relief, and to induce abortion.

Anamu — Anamu is the medicinal plant Petiveria alliacea, also called Guinea hen weed, with dibenzyl trisulfide as a prominent organosulfur bioactive linked to anticancer mechanistic work. It is best classified as a botanical extract / organosulfur natural-product source rather than a single defined drug, because published studies use crude extracts, standardized fractions, and isolated dibenzyl trisulfide. The plant is native or naturalized across tropical South and Central America, the Caribbean, parts of Africa, and the southeastern United States. Translational relevance is limited by heterogeneous extract chemistry, sparse human efficacy data, and potential reproductive, genotoxic, and hepatic safety constraints.

Primary mechanisms (ranked):

  1. Direct cytotoxic stress in cancer cells through lysosomal membrane permeabilization and caspase-independent cell death, especially shown for isolated DTS in triple-negative breast cancer models.
  2. Suppression of proliferative kinase signaling, including reported RSK1 inhibition by DTS and context-dependent MAPK axis modulation.
  3. Metabolic suppression in leukemia and tumor-cell models, including ↓ glucose uptake, ↓ oxygen consumption, ↓ intracellular ATP, and altered glycolytic / oxidative phosphorylation metabolites.
  4. ROS-linked antiproliferative stress, with ROS increase reported in some leukemia models; this appears secondary/context-dependent rather than a universal primary axis.
  5. Migration and metastasis suppression in preclinical models, linked to reduced tumor burden, reduced blast infiltration, and immune-response modulation in murine leukemia work.
  6. Immune / cytokine modulation, including older reports of Th1/Th2 cytokine switching, but this is not yet a validated oncology clinical mechanism.
  7. Chemoprevention-like CYP1A inhibition by DTS, which may reduce activation of some environmental procarcinogens but is distinct from direct tumor killing.

Bioavailability / PK relevance: Human PK for Anamu extracts or isolated DTS is not well established. Oral use is common in supplements and teas, but standardized exposure, active-metabolite formation, tissue distribution, and dose-response relationships are poorly defined. Extract identity is critical because water, ethanol, and fractionated preparations are not interchangeable.

In-vitro vs systemic exposure relevance: Most anticancer evidence is in vitro or murine, and common cell-culture concentrations may not map to achievable human plasma or tumor exposure. For crude extracts, concentration equivalence is especially weak because active DTS and other sulfur constituents vary by plant part, extraction method, and storage.

Clinical evidence status: Preclinical dominant. One registered phase Ib/II protocol is evaluating standardized Anamu extract as an adjunct with conventional therapy in metastatic gastrointestinal tumors and acute leukemias, but efficacy is not established. MSKCC states that Petiveria alliacea has not been shown to treat cancer in humans. A small osteoarthritis trial did not show benefit over placebo.

Anamu Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Lysosomal membrane permeabilization ↑ lysosomal destabilization; ↑ cathepsin-linked stress; ↑ caspase-independent death Unknown selectivity; normal-cell cytotoxicity not adequately resolved G Cell death induction Strongest modern isolated-DTS mechanism; most relevant where apoptosis resistance limits therapy response.
2 RSK1 and MAPK signaling ↓ RSK1 activity; MAPK modulation context-dependent Potential signaling effects unclear R/G Proliferation signaling disruption DTS literature emphasizes kinase inhibition or ERK/MAPK suppression; direction should be treated as context-dependent.
3 Glycolysis and oxidative phosphorylation ↓ glucose uptake; ↓ OCR; ↓ ATP; ↓ proliferative metabolites Unknown; potential energy-metabolism liability in high-demand normal tissues not defined G Metabolic growth constraint Important for leukemia models and drug-resistant tumor metabolism, but extract-specific and not yet PK-linked.
4 ROS increase secondary ↑ ROS in some leukemia models; antiproliferative stress Possible oxidative stress at high or poorly standardized exposure R/G Stress amplification ROS appears mechanistically relevant but not universal; avoid assuming NRF2 direction without model-specific data.
5 NRF2 antioxidant response ↔ insufficient direct evidence for consistent modulation ↔ insufficient direct evidence G Uncertain stress-response adaptation Do not list as a core Anamu mechanism unless a specific study reports NRF2 or downstream antioxidant targets.
6 Migration and metastasis programs ↓ migration; ↓ metastasis-related behavior; ↓ tumor burden in murine AML model Unknown G Invasion suppression Preclinical evidence supports antimetastatic potential, but clinical relevance remains unproven.
7 Immune and cytokine balance ↓ immunosuppressive tumor burden signals in murine leukemia context ↑ or ↔ cytokine modulation; Th1/Th2 shift reported historically G Host immune modulation Potential adjunctive axis; not sufficiently validated for clinical cancer use.
8 CYP1A carcinogen activation ↓ CYP1A-mediated procarcinogen activation potential ↓ CYP1A activity possible R/G Chemoprevention-like enzyme inhibition DTS was reported as a direct reversible competitive CYP1A inhibitor; this is more relevant to carcinogen activation than treatment of established tumors.
9 Cell cycle arrest ↑ growth arrest; ↓ proliferation Unknown G Antiproliferative effect Likely downstream of metabolic and kinase stress rather than an independent primary mechanism.
10 Clinical Translation Constraint Extract heterogeneity; limited human cancer efficacy data; uncertain achievable exposure Pregnancy concern; genotoxicity signals; possible liver injury; supplement quality variability G Limits clinical deployment Not an approved oncology drug; standardized clinical extract data should not be generalized to all commercial Anamu products.

P: 0–30 min R: 30 min–3 hr G: >3 hr
TumCI, Tumor Cell invasion: Click to Expand ⟱
Source:
Type:
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.
Scientific Papers found: Click to Expand⟱
6602- Anamu,    Dibenzyl Trisulfide Inhibits the Proliferation and Metastasis of Nsclc Via Suppressing Jak/Stat3 Signal Pathway
- vitro+vivo, NSCLC, H1299 - in-vitro, NSCLC, A549
TumCP↓, TumCMig↓, TumCI↓, Apoptosis↑, BAX↑, Bcl-2↓, EMT↓, p‑STAT3↓, TumCG↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   p‑STAT3↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCI, Tumor Cell invasion
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#:193  Target#:324  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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