Allicin (mainly Garlic) / AntiAg Cancer Research Results

AL, Allicin (mainly Garlic): Click to Expand ⟱
Features:
Garlic (Allium sativum L.) (active ingredient- Allicin, an active sulfer compound).

Allicin — a reactive organosulfur thiosulfinate generated in situ when garlic (Allium sativum) tissue is crushed (alliin → allicin via alliinase). Functionally, it behaves as a short-lived electrophilic “reactive sulfur species” that rapidly modifies cellular thiols (e.g., glutathione and cysteine residues on proteins), producing broad redox and stress-signaling effects. Classification: small-molecule phytochemical (organosulfur thiosulfinate). Source/origin: freshly crushed raw garlic; allicin is not present in intact cloves and is chemically unstable, converting to other organosulfur metabolites after formation.

Primary mechanisms (ranked):

  1. Thiol reactivity and redox disruption: rapid GSH/protein-thiol modification (S-thioallylation), shifting redox buffering and triggering oxidative/electrophilic stress signaling.
  2. Mitochondrial stress and intrinsic apoptosis (context-dependent): ΔΨm disruption, cytochrome-c release, caspase activation, ER stress/UPR engagement (often downstream of redox stress).
  3. Inflammatory transcriptional suppression (context-dependent): inhibition of NF-κB–linked programs and, in some models, STAT3 signaling.
  4. Acetate metabolism constraint (model-dependent): reversible inhibition of acetyl-CoA synthetase activity (ACS/ACSS), potentially impacting acetate→acetyl-CoA flux under metabolic stress.
  5. Growth and invasion signaling attenuation (model-dependent): PI3K/AKT and MAPK network modulation with downstream effects on EMT/MMPs and angiogenic programs (e.g., HIF-1α/VEGF).

Bioavailability / PK relevance: “Allicin exposure” is dominated by formation conditions and rapid chemical/biologic turnover. Many oral preparations deliver alliin/alliinase that may generate allicin after ingestion; measured systemic allicin is typically transient, while downstream allyl-sulfur metabolites (e.g., allyl methyl sulfide–related products) are more detectable. Cooking/processing and GI conditions substantially change allicin bioequivalence versus crushed raw garlic.

In-vitro vs systemic exposure relevance: Many anticancer cell studies use ~50–300 µM allicin; whether such free allicin concentrations are achievable at tumor sites after dietary/supplement intake is uncertain because of rapid thiol quenching and conversion to other sulfur species. Reported biological effects at lower concentrations may still occur locally (GI lumen/mucosa) or via metabolites, but direct extrapolation from high-µM in-vitro dosing is high-risk.

Clinical evidence status: Predominantly preclinical (cell/animal) for anticancer mechanisms; human data are mixed and often evaluate garlic preparations rather than purified allicin, with outcomes confounded by formulation-dependent “allicin bioequivalence” and co-occurring organosulfur compounds (e.g., DADS/DATS/SAMC). Cancer-therapeutic evidence remains inconclusive.

DADS (diallyl disulfide is a sulfur-based anticancer drug generated from garlic)
Summary:
- Four main organic sulfides in garlic, diallyl disulfide (DADS), diallyl trisulfide (DATS), S-allylmercaptocysteine (SAMC) and allicin.
- Reversible inhibitor of ACSS2.
- may inhibit NF-κB signaling
- induce oxidative stress in cancer cells by generating ROS
- might downregulate STAT3 activation
- Inconclusive evidence for cancer treatment.
- may inhibit platelet aggregation
Allicin is a reactive sulfur species (RSS) [23] with oxidizing properties, and it is able to oxidize thiols in cells, e.g., glutathione and cysteine residues in proteins.
-Allicin is not present in intact garlic; rather, it is formed when garlic is chopped or crushed. -Using crushed or chopped raw garlic or adding garlic at the end of the cooking process (after the heat is reduced) can help preserve its potential allicin content.
"Consumption of alliinase-inhibited cooked garlic was found to give higher than expected allicin bioequivalence, with AMS formation being about 30% (roasted garlic) or 16% (boiled garlic) that of crushed raw garlic."

-Allicin is not present in intact garlic.
-It's formed enzymatically when alliin (a sulfur-containing amino acid) is converted by alliinase when garlic is chopped or crushed.Best consumed raw immediately after crushing (wait 5–10 min before consuming for full conversion)
-Allicin is unstable, degrading within hours into other sulfur compounds (like diallyl disulfide).

-Note half-life reports vary 2.5-90hrs?.
-moderately water-soluble but rapidly degrades/quenched (especially with thiols), so aqueous solutions have limited practical stability : BioAv


Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.
- inhibit Growth/Metastases : EMT↓, MMP2↓, MMP9↓, VEGF↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓(not commonly listed as inhibitor), DNMT1↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, FAK↓, ERK↓,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- inhibits Cancer Stem Cells : CSC↓,
- Others: PI3K↓, AKT↓, STAT3, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Allicin has been reported to exhibit a range of effects, including:
Antimicrobial activity: 10-50 μM
Antioxidant activity: 10-100 μM
Anti-inflammatory activity: 20-50 μM
Anticancer activity: 50-100 μM or (50–300uM) (2–5 mg allicin per kilogram of body weight per day)
Cardiovascular health: 20-50 μM

Approximate μM concentrations of allicin that can be achieved:
1 clove of garlic (3g): approximately 10-50 μM of allicin
single clove of garlic may yield about 5–9 mg of allicin,
1 tablespoon of minced garlic (15g): approximately 50-150 μM of allicin
1 cup of chopped garlic (100g): approximately 200-500 μM of allicin
1 tablespoon of chopped garlic chives (15g): approximately 5-20 μM of allicin
1 cup of chopped garlic chives (100g): approximately 20-50 μM of allicin
1 ounce (28g) of garlic microgreens: approximately 50-200 μM of allicin
1 cup of garlic microgreens (100g): approximately 200-500 μM of allicin
1 ounce (28g) of garlic chive microgreens: approximately 20-50 μM of allicin
1 cup of garlic chive microgreens (100g): approximately 50-100 μM of allicin

Allicin is a bioactive compound derived from garlic that has garnered significant interest for its potential anticancer properties through multiple mechanisms, including antioxidant activity, induction of apoptosis, cell cycle arrest, and modulation of key signaling pathways. While regular dietary intake of garlic is associated with cancer prevention benefits, allicin is also being explored as an adjunct to conventional cancer treatments.

Available in supplement tablet/capsule form for example at 2000mg (fresh bulb equilvalent)
IC50 of normal cells it >160mg/mL (large selectivity).
IC50 might be about 12-30ug/ml (approximately 62-185 µM) (which is about 30-90 grams of garlic consumption).
This makes it difficult to consume enough supplements to achieve that level.

Pathways:

ROS Generation and Oxidative Stress (inducing)
• ROS generation is often considered a primary trigger that feeds into downstream pathways (e.g., MAPK activation, mitochondrial membrane permeabilization).
Mitochondrial (Intrinsic) Apoptotic Pathway
• ROS-induced mitochondrial damage can lead to the release of cytochrome c and subsequent activation of caspases (e.g., caspase-9 and caspase-3).
NF-κB Signaling Inhibition (block)
Modulation of MAPK Pathways (e.g., p38 MAPK and JNK)
• ROS generation by allicin can activate stress-responsive kinases such as p38 MAPK and c-Jun N-terminal kinase (JNK).
Inhibition of PI3K/Akt Pathway
ROS levels and PI3K/Akt signaling, with increased oxidative stress often correlating with reduced Akt phosphorylation and activity.

At lower doses, allicin may lead to a modest increase in ROS levels that the cell’s antioxidant defenses (e.g., glutathione, superoxide dismutase) can manage

Allicin (Garlic) — mechanistic axes relevant to oncology

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Thiol chemistry and redox buffering GSH↓, protein thiols modified; ROS↑ (dose-dependent) Adaptive buffering often stronger; ROS↔/↑ (context-dependent) P Electrophilic/thiol stress that re-wires signaling Central “first-contact” mechanism: allicin rapidly reacts with cysteine/GSH, so many downstream pathway changes are secondary to thiol stress.
2 Mitochondria and intrinsic apoptosis ΔΨm↓, Cyt-c↑, Caspase↑, cl-PARP↑ Typically less apoptosis at matched doses (selectivity varies) R Pro-apoptotic stress execution Frequently downstream of rank #1; selectivity can reflect baseline redox fragility and metabolic state.
3 ER stress and UPR ER stress↑, UPR↑ (model-dependent) UPR↔/↑ (context-dependent) R Proteostasis stress amplification Can couple to Ca²⁺ release, apoptosis, and inflammatory signaling changes.
4 Ca²⁺ signaling Ca²⁺↑ (model-dependent) Ca²⁺↔/↑ (context-dependent) R Stress coupling to mitochondria/ER Often reported as part of the ER–mitochondria stress axis rather than a primary target.
5 NF-κB inflammatory axis NF-κB↓; cytokine programs↓ (context-dependent) Inflammatory tone↓ (context-dependent) G Anti-inflammatory transcriptional suppression May be beneficial in tumor-promoting inflammation contexts; also relevant to platelet/vascular biology.
6 STAT3 signaling STAT3↓ (model-dependent) STAT3↔ (context-dependent) G Reduced survival/proliferation programs Evidence is model-specific; frequently downstream of redox/inflammation modulation.
7 NRF2 antioxidant response NRF2↓ or maladaptive NRF2 response (context-dependent) NRF2↑ (context-dependent) G Differential stress adaptation Reported “cancer vs normal” divergence is plausible but not universal; strongly dose/model dependent.
8 Acetate to acetyl-CoA metabolism ACS/ACSS activity↓ (model-dependent) ACS/ACSS activity↓ (context-dependent) R Limits acetate utilization under stress Primary biochemical evidence exists for acetyl-CoA synthetase inhibition by allicin; translation to tumor-selective ACSS2 targeting is uncertain without exposure confirmation.
9 PI3K/AKT and MAPK network PI3K/AKT↓, ERK/JNK↔/↓ (model-dependent) ↔ (context-dependent) G Reduced growth/survival signaling Commonly reported but typically secondary to upstream stress/redox effects.
10 HIF-1α and angiogenesis HIF-1α↓, VEGF↓ (model-dependent) ↔ (context-dependent) G Anti-angiogenic signaling shift Most supportive data are preclinical; dependent on hypoxia models and dosing.
11 EMT, migration, invasion EMT↓, MMPs↓ (model-dependent) ↔ (context-dependent) G Reduced invasive phenotype Usually downstream of PI3K/MAPK/inflammation rewiring and/or oxidative stress–driven cytostasis.
12 Radiosensitization and chemosensitization Sensitization↑ (context-dependent) Protection↔/↑ (context-dependent) G Stress-based therapeutic interaction Potential bidirectionality: pro-oxidant sensitization in tumors vs antioxidant adaptation in normal tissues depends on schedule and formulation.
13 Clinical Translation Constraint Chemical instability; rapid thiol quenching; formulation-dependent “allicin bioequivalence”; uncertain tumor-site free-allicin exposure; many in-vitro studies use high µM levels; human cancer outcomes largely from heterogeneous garlic preparations rather than purified allicin. Primary constraint is exposure control, not target plausibility.


AntiAg, Antiplatelet aggregation: Click to Expand ⟱
Source:
Type:
Antiplatelet aggregation refers to the process by which platelets clump together to form a blood clot.
The plethora of evidence indicates that among multiple hemostasis components, platelets play major roles in cancer progression by providing surface and granular contents for several interactions as well as behaving like immune cells.On the other hand, there are suggestions that antiplatelet treatment may promote solid tumor development in a phenomenon described as “cancers follow bleeding.” The controversies around antiplatelet agents justify insight into the subject to establish what, if any, role platelet-directed therapy has in the continuum of anticancer management.
The interplay between antiplatelet aggregation and cancer is an area of active research, with potential implications for therapeutic strategies. Antiplatelet agents, such as aspirin, are being investigated for their role in cancer prevention and treatment, particularly in reducing metastasis and improving patient outcomes.
Scientific Papers found: Click to Expand⟱
2658- AL,    The Toxic Effect Ways of Allicin on Different Cell Lines
- Review, Var, NA
*antiOx↑, The significant functional act of garlic is its anticancer, antimicrobial, antioxidant, antidiabetic, antifibrinolytic, immune enhancing, antiplatelet collected effect and its possible act in prohibiting cardiovascular illnesses
*AntiAg↑,
*cardioP↑,
Ca+2↑, Sultan et al.[34] stated that allicin is cytotoxic to monocytic leukemia cells (THP-1 cells) and stimulates calcium-linked hemolysis and eryptosis in human red blood cells. Allicin advances calcium grades in cells, reasons to oxidative stress and al
ROS↑, Allicin advances calcium grades in cells, reasons to oxidative stress and also induces CK1a, caspase, p38, mitogen-activated protein kinase
Casp↑,
p38↑,
MAPK↑,
hepatoP↑, Wu et al.[42] clarified that allicin applies hepaprotective action counter to hepatic toxicity of cells
chemoP↑, Throughout with other garlic preparations, aged garlic extract (AGE) has been indicated to have hepatoprotective, immune, improving, anticancer, and chemoprotective actions.

2560- AL,    Effect of garlic on platelet aggregation in humans: a study in healthy subjects and patients with coronary artery disease
- ex-vivo, Nor, NA
*AntiAg↑, Garlic and its components are known to possess antiplatelet activity
BioAv↝, Though garlic components leave the body quickly, a slow build-up of the active ingredients may take place.
Dose↝, Each capsule contained oil equivalent to I g of raw garlic. oil extract of garlic was encapsulated. 2 capsules of garlic three times a day (i.e. 6 capsules/day) for a period of 1 month.

2559- AL,    Effect of the Garlic Pill in comparison with Plavix on Platelet Aggregation and Bleeding Time
- Human, Nor, NA
AntiAg↑, Several studies indicated that garlic can inhibit platelet aggregation
COX2↓, garlic prevents inhibition of platelet aggregation by inhibiting cyclooxygenase activity and thus thromboxane A2 (TXA2) and B2 (TXB2
cardioP↑, Garlic can play an effective role in preventing and treating cardiovascular diseases.

7153- AL,  Gins,  GI,  VitE,  Lyco  Anticoagulant activity of select dietary supplements
- Review, Nor, NA
*AntiAg↑, Garlic Reduces ADP-induced platelet aggregation; thromboxane reduction; reduces clotting time
other?, Ginseng Inhibits thromboxane function
other?, Ginger Alters thromboxane synthesis; inhibits arachidonic acid-induced platelet activation
other?, Vitamin E Reduces platelet adhesion to endothelial cells; increases bleeding time; prevents platelet aggregation
other?, Lycopene Inhibits platelet aggregation

7148- AL,  VitE,  Se,    Antithrombotic effects of naturally derived products on coagulation and platelet function
- Review, Nor, NA
*AntiAg↑, The sulfuric compound responsible for the distinct odor of garlic, allicin, appears to be primarily responsible for the inhibitory effect of garlic on platelet aggregation
*other↑, Along with its antioxidant properties, vitamin E has multiple antiplatelet properties that appear to be independent of its antioxidant activitie
*other↑, Therapies aimed at increasing the levels of selenium in the body result in the inhibition of platelet aggregation, primarily through thromboxane A2

7146- AL,  GI,  Eug,  CAP,    Herbal remedies and anticoagulant therapy
- Review, Nor, NA
*AntiAg↑, The allicin derivative of garlic root has been shown to enhance fibrinolytic activity and inhibit platelet aggregation in patients with coronary artery disease
*PGE2↓, Other herbs may also affect platelet function through inhibition of prostaglandin metabolism. Ginger, used by pregnant women for the relief of nausea and vomiting
*AntiAg↑, while clove – a common kitchen spice and important source of dietary antioxidants (60), contains two antiplatelet components (eugenol and acetyl eugenol) which inhibit platelet thromboxane formation and increase formation of 12-HPETE
*TXA2↓,
*AntiAg↑, Red pepper (capsaicin), an herb used to alleviate diabetic neuropathy (74), inhibits both platelet aggregation and release (75), as well enhancing fibrinolytic activity

6763- AL,    Revealing the Therapeutic Uses of Garlic (Allium sativum) and Its Potential for Drug Discovery
- Review, Nor, NA
*Inflam↓, It has anti-inflammatory, rheumatological, ulcer inhibiting, anticholinergic, analgesic, antimicrobial, antistress, antidiabetes, anticancer, liver protection, anthelmintics, antioxidants, antifungal, and wound healing propertie
*AntiBio↑,
*AntiDiabetic↑,
*hepatoP↑,
*antiOx↑,
*AntiFungal↑,
*Wound Healing↑,
*other↑, Garlic has a higher concentration of sulfur compounds (allicin, diallyl disulfide, S-allylcysteine, and diallyl trisulfide), which are responsible for its therapeutic properties.
*BP↓, Garlic consumption lowers blood pressure, inhibits atherosclerosis, decreases serum cholesterol and triglycerides, suppresses platelet aggregation, and increases fibrinolytic activity, among other things
*LDL↓,
*AntiAg↑,
*cognitive↑, Garlic can also aid in preventing cognitive decline by shielding neurons from neurotoxicity and apoptosis, which helps to prevent ischemia, obsessive-compulsive disorder (OCD), and neuronal death while also boosting learning and memory retention
*memory↑,
Risk↑, People who consumed more garlic had a 54% decreased risk of pancreatic cancer than those who consumed fewer amounts of garlic
*COX1↓, Garlic supplements have been demonstrated to reduce cyclooxygenase activity and thromboxane A2 production, resulting in antiplatelet action
*TXA2↓,

5353- AL,    Aged Garlic Extract May Be Safe for Patients on Warfarin Therapy
- Human, Nor, NA
*AntiAg↑, Garlic has been known to have antiplatelet properties.
*toxicity↓, The results suggest that AGE is relatively safe and poses no serious hemorrhagic risk for closely monitored patients on warfarin oral anticoagulation therapy.
*cardioP↑, ts positive effects may be beneficial to people with a high-risk background or who are taking cardiovascular medications
*Dose↝, formulated by soaking sliced raw garlic in aqueous ethanol solution for up to 20 mo at room temperature. The extract was filtered and concentrated under reduced pressure at low temperature

2558- AL,    Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment
- Review, AD, NA
*AntiCan↑, Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases
*antiOx↑,
*cardioP↑,
*neuroP↑, present review describes allicin as an antioxidant, and neuroprotective molecule
cognitive↑, that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders.
*ROS↓, As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases.
*NOX↓,
*TLR4↓, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways.
*NF-kB↓,
*JNK↓,
*AntiAg↑, A low concentration of allicin (0.4 mM) can inhibit the platelet aggregation up to 90%, the impact is significantly higher than of similar concentration of aspirin.
*H2S↑, Allicin decomposes rapidly and undergoes a series of reactions with glutathione resulting in the production of hydrogen sulphide (H2S).
*BP↓, H2S is a gaseous signalling molecule involved in the regulation of blood pressure.
Telomerase↓, Allicin inhibits the activity of telomerase in a dose dependent manner subsequently inhibiting the proliferation in the cancer cells
*Insulin↑, Studies have shown a significant increase in the blood insulin levels after treatment with allicin
BioAv↝, optimum temperature for the activity of alliinase is 33 °C, it operates best at pH 6.5, the enzyme is sensitive to acids [42,43] (Figure 3), enteric-coated formulations of garlic supplements are therefore recommended
*GSH↑, It helps to lower the hyperglycaemic conditions and improves the glutathione and catalase biosynthesis [37,38]
*Catalase↑,

2463- AL,    Garlic as an antithrombotic and antiplatelet aggregation agent
- Review, Nor, NA
AntiAg↑, This review suggests that garlic and its preparations have a beneficial effect against thrombosis and have an antiplatelet aggregation property.
other↑, Garlic been shown to inhibit platelet aggregation, both in vivo and in vitro

2462- AL,    Comparison of antiplatelet activity of garlic tablets with cardio-protective dose of aspirin in healthy volunteers: a randomized clinical trial
- Trial, Nor, NA
AntiAg∅, Garlic tablet did not have significant effect on PA at any dose.


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Cell Death(tgid=5) ⓘ

Casp↑, 1,   MAPK↑, 1,   p38↑, 1,   Telomerase↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other?, 4,   other↑, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 2,   AntiAg∅, 1,   Ca+2↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 2,   Dose↝, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   chemoP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   Risk↑, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 1,   GSH↑, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

Insulin↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

H2S↑, 1,   LDL↓, 1,  

Cell Death(tgid=5) ⓘ

JNK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 3,  

Migration(tgid=13) ⓘ

AntiAg↑, 10,  

Angiogenesis & Vasculature(tgid=14) ⓘ

TXA2↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   Inflam↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TLR4↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BP↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiDiabetic↑, 1,   cardioP↑, 3,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   toxicity↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,  
Total Targets: 30

Scientific Paper Hit Count for: AntiAg, Antiplatelet aggregation
11 Allicin (mainly Garlic)
2 Ginger/6-Shogaol/Gingerol
2 Vitamin E
1 Ginseng
1 Lycopene
1 Selenium
1 Eugenol
1 Capsaicin
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#:27  Target#:10  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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