BioEnh Cancer Research Results

BioEnh, bioenhancer: Click to Expand ⟱
Source:
Type:
A bioenhancer is an agent capable of enhancing bioavailability and efficacy of a drug with which it is co-administered

Query Database for BioEnhancers but the bioenhancers mainly show up under the target notes

Bioenhancers
- piperine and quercetin are considered bio-enhancers
- genistein
Piperine act by suppressing P-gp and cytochrome P450 enzymes, which counteract the metabolism of rifampicin via these proteins, thus enhancing the oral bioavailability of rifampicin. It also decreases the intestinal production of glucuronic acid, thus allowing more substances to enter the body in active form. It was found to increase the bioavailability of various drugs from 30% to 200%.[25]
Table 1: Published research on bioenhancer effect of piperine with various medicines
Drug Studied in Reference
Antimicrobial agents
Rifampicin In vitro Balakrishnan et al, 2001[11]
Isoniazid Rabbits Karan et al, 1998 [12]
Pefl oxacin Mountain Gaddi goats Madhukar et al, 2008[13]
Tetracycline Rats Atal et al, 1980[14]
Sulfadiazine Rats and dogs Atal et al, 1980[14]
Oxytetracycline Poultry birds Singh et al, 2005[15]
Ampicillin Rabbits Janakiraman and Manavalan, 2008[16]
Norfl oxacin Rabbits Janakiraman and Manavalan, 2008 [16]
Nevirapine Adult males Kasibhatta et al, 2007 [17]
Metronidazole In vitro Singh et al, 2010[18]
Analgesics
Diclofenac sodium Albino mice Pooja et al, 2007[19]
Pentazocine Albino mice Pooja et al, 2007[19]
Nimesulide Mice Gupta et al, 1998[20]
Antiepileptics
Carbamazepine In vitro Pattanaik et al, 2009 [21]
Phenytoin Human volunteers Bano et al, 1987[22]
Pentobarbitone Rats Majumdar et al, 1990[23]
Other drugs
Propranolol In vitro Bano et al, 1991 [24]
Theophylline In vitro Bano et al, 1991 [24]
Nutrients In vitro Pooja et al, 2007 [19
***Borneol
-Borneol is thought to temporarily open tight junctions between endothelial cells, enhancing drug penetration. It may also downregulate efflux transporters such as P-glycoprotein (P-gp), allowing higher intracellular concentrations of co-administered drugs.

-presence of urea (as a carrier) increased the aqueous solubility of capsaicin by 3.6-fold compared to pure capsaicin

Quercetin is found in citrus fruits and is a dual inhibitor of cytochrome P 3A4 (CYP3A4) and P-gp.
Table 2: Effect of quercetin pretreatment/co-treatment on pharmacokinetic parameters of different drugs
Drugs combined Increase in pharmacokinetic parametera
Cmax AUC ABA
Verapamil Two fold Two fold SH
Diltiazem SH SH Not known
Paclitaxel SH SH T wo fold
Digoxin 413% 170% Not known
Tamoxifen SH SH 59%
Compared to drug in question alone. Cmax, peak plasma concentration; AUC, area under the curve; ABA, absolute bioavailability; SH, significantly higher.

Another flavonoid, genistein belongs to the isoflavone class of flavonoids. It is a well-known phytoestrogen. The presence of genistein (10 mg/kg) caused an increase in AUC (54.7%) and a decrease in the total plasma clearance (35.2%) after oral administration of paclitaxel at a dose of 30 mg/kg in rats.[37]
Naringin is the major flavonoid glycoside found in grapefruit and makes grapefruit juice taste bitter. Oral naringin (3.3 and 10 mg/kg) was pretreated 30 min before and after intravenous administration of paclitaxel (3 mg/kg), the AUC was significantly improved (40.8% and 49.1% for naringin doses of 3.3 and 10 mg/kg, respectively).[38

Carum carvi/Cuminum cyminum ( Jeera)
Carum carvi seeds are a prized culinary herb. Extracts of its parts increased significantly (25%–300%), the bioavailability of a number of classes of drugs, such as antibiotics, antifungals, antivirals, anticancer, cardiovascular, anti-inflammatory/ antiarthritic, anti-TB, antileprosy, antihistaminic/respiratory disorders, corticosteroids, immunosuppressants, and antiulcers. Such extracts either in the presence or absence of piperine have been found to be highly selective in their bioavailability/bioefficacy-enhancing action.[40]
Capmul
One of the widely used bioenhancers is Capmul MCM C10, a glyceryl monocaprate, produced from edible fats and oils and is commonly used in lip products. In a study in rats, antibiotic ceftriaxone when given concomitantly with capmul, increased the bioavailability of ceftriaxone by 80%.[41]
Nitrile glycoside
Nitrite glycoside is a bioenhancer for drugs and nutrients. Novel bioactive nitrile glycosides, niaziridin and niazirin is obtained from the leaves, pods, and bark of Moringa oleifera. [42] An immunoenhancing polysaccharide and niaziminin, having structural requirement to inhibit tumor promoter-induced Epstein–Barr virus activation have been reported from the leaves of Moringa.[43,44] It enhances the bioactivity of commonly used antibiotics, such as rifampicin, tetracycline, and ampicillin, and also facilitate the absorption of drugs, vitamins, and nutrients through the gastrointestinal membrane, thus increasing their bioavailability. [41] Niazirin is another bioactive nitrile glycoside belonging to M. oleifera. [45,46] Process of isolation of nitrite glycoside from M. oleifera has been patented (US 6858588) by Khanuja et al in 2004–2005. [42

Mechanism of Action Of Bioenhancers
Bioavailability-enhancing activity of natural compounds from the medicinal plants may be attributed to various mechanisms, such as P-gp inhibition activity by flavone, quercetin, and genistein; [51] inhibition of efflux transporters, such as P-gp and breast cancer resistance protein (BCRP),[52,53] by naringin and sinomenine thus preventing drug resistance; DNA receptor binding, modulation of cell signaling transduction, and inhibition of drug efflux pumps[54-56] ; by stimulating leucine amino peptidase and glycyl–glycine dipeptidase activity, thus modulating the cell membrane dynamics related to passive transport mechanism as seen with piperine [57] ; nonspecific mechanisms, such as increased blood supply to the gastrointestinal tract, decreased hydrochloric acid secretion, preventing breakdown of some drugs[6] ; and inhibition of metabolic enzymes participating in the biotransformation of drugs, thus preventing inactivation and elimination of drugs and thereby, increasing their bioavailability. [57-5]


AD, Alzheimer's Disease: Click to Expand ⟱
In Alzheimer's disease (AD), cholinergic dysfunction (often with reduced acetylcholine tone and impaired choline metabolism) is linked with cortical dysfunction, memory deficit, abnormal cerebral blood flow, task learning difficulty, sleep-cycle disruption, and neurodevelopmental effects (context-dependent).
CORE HALLMARKS / HIGH-CONFIDENCE AXES:
- tau and Aβ, their accumulation in AD brains is known to be a major hallmark.
  In AD, PP2A↓ activity is decreased (reported), contributing to hyperphosphorylated tau accumulation.
  SIRT-1↓ levels in AD brains are associated with accumulation of Aβ and tau (reported).
- glucose metabolism↓ (brain glucose hypometabolism) occurs in AD long before significant clinical signs in many cohorts/models (reported).
- Neuroinflammation / lipid mediator tone (reported): 5-LOX↑ and PGE2↑ (model-/region-dependent).
- Synaptic vulnerability (reported): PSD95↓ in hippocampus and cortex; restoring PSD95 shows cognitive benefits in models.
- Clearance/transport imbalance (reported): IDE↓, NEP↓, LRP1↓, and AEP↑ protein levels in AD brains (reported).

COMMONLY REPORTED DIRECTIONAL CHANGES (model/region/compartment dependent):
- Monoamines (reported): concentrations of 5-HTP↓, 5-HT(seratonin)↓, and 5-HIAA↓ are lower in Alzheimer's patients (varies by region/study).
- Cholinergic system (clinical target): reduction in ACh↓ production; ChAT↓ activity reduced (synthesizes ACh).
- Four key enzymes frequently targeted in AD symptom/adjunct strategies: AChE, BChE, MAOA, MAOB (objective inhibit).
- Neurotrophic tone (reported): BDNF↓ in key regions.
  - Stress can decrease expression of brain-derived neurotrophic factor (BDNF).
- Kinase/protease stress (reported): CDK5↑ hyperactivation; calpain↑ overactivated by increased intracellular Ca²⁺ → p-tau and aggregation.
- Aβ-linked synaptic regulator (reported): STEP↑ upregulated largely due to Aβ oligomer accumulation.
- α-secretase axis (reported): ADAM10↓ downregulated in AD brains.
- Metabolic cofactors (reported): ALC↓ (ALCAR); Homocarnosine↓ (CSF declines with age); possible low Taurine↓ (age-related + dementia reports).
- Ion/glutamate handling (reported): impaired glutamate clearance + depressed Na+/K+ ATPase → cellular ion imbalance risk.
- Aging reduces NAD⁺↓ (in AD depletion may be more severe).
- Mitochondrial capacity axis (reported): PGC-1↓ decreased in Alzheimer’s brains.
- Innate immune DNA-sensing axis (animal): cGAS–STING↑ elevation observed in AD mice and normalized by NR treatment.
- Vascular/structure (reported): a profound change in BBB permeability; progressive brain shrinkage (atrophy).
- Glycation axis (reported): AGEs↑ and RAGE↑ expression.

HOMOCYSTEINE / B-VITAMIN AXIS:
- Raised plasma total homocysteine (tHcy)↑ associated with cognitive impairment, AD, or vascular dementia (epidemiology).
  - Homocysteine can build up if vitamin B6, B12, or folate levels are low.
  - Homocysteine and B-vitamin in Cognitive Impairment (VITACOG) study.
  - Vit B6 might be an important B vitamin (often discussed along with B12 and folate).
- Thiamine↓ deficiency produces a cholinergic deficit (well-aligned with AD features).
- Decreased thiamine (B1) in AD may exacerbate Aβ deposition, tau hyperphosphorylation, and oxidative stress (reported).

MICRONUTRIENTS / CAROTENOIDS (reported; compartment-dependent):
- vitamin A↓ and β-carotene↓ lower in some AD cohorts; excess retinol may contribute to osteoporosis risk.
- Diminished circulating vitamin E↓ reported in AD.
- Vitamin B5↓ in multiple brain regions (reported).
- Trace elements: patients with AD reported lower serum Se, Cu, and Zn↓ (serum findings vary by study).
- Brain metals: some studies report higher brain copper↑ and iron↑ in specific regions/structures; compartment and region matter.
  Rosmarinic acid reported to reduce copper-induced neurotoxicity in vitro/in vivo and may interfere with amyloid–copper interactions (preclinical).
- SAMe↓ concentrations in CSF reported in AD.
- MPOD often reduced in AD patients.
- AD brains reported lower levels of lutein↓, zeaxanthin↓, anhydrolutein↓, (VitA)retinol↓, lycopene↓, alpha-tocopherol↓.

RISK CONTEXT:
- Apolipoprotein E4 (ApoE4) genotype is the strongest known genetic risk factor for late-onset AD.
  - One copy of ApoE4: ~3–4× increased risk (range varies by cohort).
  - Two copies: ~8–12× increased risk (range varies).
  - VitK lower in circulating blood of APOE4 carriers (reported).
- Type 2 diabetes, traumatic brain injury, stroke, diet, and above all, aging is the number ONE risk factor.

Treatments / Strategy Targets (high-level):
- Early intervention tends to have a greater positive effect than interventions during middle or late stages.
- BOLD fMRI imaging can be used to observe brain activity via blood oxygen/flow changes.
- Reduce ROS and inflammation in the brain (context-dependent; avoid over-suppressing adaptive signaling).
- Inhibiting acetylcholinesterase (AChE) (which breaks down ACh), e.g., donepezil, rivastigmine.
- Natural AChE inhibitors include: Berberine, Luteolin, Crocetin(saffron), Querctin, TQ
- Natural AChE inhibitors in database (check BBB pass potential).
- MAOB inhibitors, APP inhibitors, PGE2 inhibitors, NLRP3 inhibitors, BACE inhibitors
- BDNF activators, PSD95 activator
- STEP, ADAM10
- Diets with an adequate ratio (5:1) of omega-6:3 (Mediterranean diet).
- Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects (general nutrition framing).
- Antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin).
- Fiber may promote gut microbiome diversity influencing brain health.
- Supplementing with NAD⁺ precursors (NR or NMN) improves cognition and reduces amyloid/tau pathologies in AD mice (animal evidence).
- "It is advisable to consume diets with an adequate ratio (5:1) of omega-6:3 fatty acids (Mediterranean diet) ... antioxidants ... role in oxidative stress ... cognition." Nutrition Strategies
- Reduction of cognitive decline may be achieved by following a healthy dietary pattern limiting added sugars while maximizing fish, fruits, vegetables, nuts, seeds.

SeNPs may also be useful as a Drug Delivery System.


Related Pathways to research in this database (products that modulate them):
- neuroprotective, cognitive, memory
- Aβ aggregation, Tau↓, AChE↓, ACh↑, ChAT↑, acetyl-CoA↑, BDNF↑, BACE↓, NLRP3↓, PSD95↑, PGE2↓, homoC↓
- Increasing AntiOxidants: Catalase↑, GSH↑, SOD↑, HO-1↑, to decrease ROS↓
- Lower Inflammation: TNF-α↓, IL1β↓, IL6↓

Natural Products that may benefit AD.
-Some key pathways are highlighted in RED in the following links
Acetyl-L-carnitine, ALA, Apigenin, Anthocyanins Blueberrys, Aromatherapy, Artemisinin, Ashwagandha,
β-carotene(vitamin A), Bacopa monnieri, Baicalein, Baicalin, Berberine, Betulinic acid, Boron, Boswellia (frankincense),
Caffeic acid, Caffeine, Capsaicin, Carnosine, Carnosic acid, Chlorogenic acid, Choline, Chrysin, Cinnamon, CoQ10, Crocetin, Curcumin,
dietMed, dietMet, dietSTF, EGCG, Ellagic acid, Exercise, Ferulic Acid, Fisetin, Flav, FLS, Folic Acid (5-MTHF, L-methylfolate)-reduce homocysteine,
Galantamine, Ginger, Ginkgo biloba, Ginseng,
Honokiol, Huperzine A, hydrogen gas, Lecithin, Lutein, Luteolin, Lycopene,
M-Blu, Moringa oleifera, Mushroom Lion’s Mane, MSM, MCToil, NAD, Naringenin,
PEMF, Piperine, Phenylbutyrate, Phosphatidylserine, Piperlongumine, Potassium, probiotics, Propolis, Pterostilbene,
Quercetin, Resveratrol, Rivastigmine, Rosmaric Acid(reduce copper-induced neurotoxicity), Rutin,
Safflower yellow, Sage, SAMe, selenium, Serotonin, Shankhpushpi, Shikonin, Shilajit/Fulvic Acid, silicon(reduce Alum bioavialability), Silymarin (Milk Thistle) silibinin, Sulforaphane,
Taurine, TQ, Ursolic Acid
Vitamin B1, Vitamin B2, Vitamin B3, Vitamin B5, Vitamin B6, Vitamin B12, Vitamin E, Vitamin D, Vitamin K2
Zeaxanthin, zinc,

Aluminium has a negative impact on cognition but silicon can decrease Alumunium bioavailability, and Vitamin K2 may provide some protection. Example So does RMF

Brain Energy Systems Matrix (AD)

Tier 1–2 as “core metabolic cofactors / redox pools”
Tier 4 as “alternative fuels / bypass strategies”
Tier 5–6 as “capacity + delivery constraints” (often explains why supplements don’t translate)
Tier Rank Node / Lever What it Supports (Bioenergetic Role) Key Enzymes / Targets AD-Relevant Mechanism TSF Evidence Common Constraints / Gotchas
11 Thiamine (B1) / TPP Glucose → acetyl-CoA entry + TCA throughput + NADPH support PDH, α-KGDH, Transketolase (PPP) Addresses cerebral glucose hypometabolism; improves mitochondrial flux; PPP→NADPH supports redox R, G Mechanistic + small clinical Benefit strongest if low status; standard thiamine vs lipophilic derivatives differ
12 Benfotiamine Higher-bioavailability B1 strategy Transketolase ↑; glycation axis ↓ AGE/RAGE burden reduction + metabolic support (model/trial dependent) G Small clinical + mechanistic Not a “rapid” effect; mostly longer-term metabolic/toxicity load reduction
13 Riboflavin (B2) / FAD, FMN ETC redox enzymes + mitochondrial dehydrogenases Complex I/II flavoproteins; many oxidoreductases Supports electron handling; can be limiting in mitochondrial enzyme insufficiency R, G Mechanistic Direct AD cognitive trial support limited; “helps” mostly when deficient or enzyme-limited
14 Niacin forms (B3) → NAD pool NAD+/NADH redox + signaling + repair NAD salvage; sirtuins; PARP substrate NAD decline is an aging/inflammation theme; supports mitochondrial redox capacity R, G Emerging human + mechanistic Different forms behave differently; NAD raising ≠ guaranteed clinical cognition benefit
15 Pantothenic acid (B5) → CoA Acetyl-CoA formation; lipid metabolism; TCA entry CoA biosynthesis; acetylation capacity Foundational for fuel oxidation and acetylation balance G Mechanistic Often overlooked; deficiency uncommon but suboptimal intake can matter in frailty
16 Magnesium ATP handling (Mg-ATP) + enzyme kinetics ATP-dependent enzymes; synaptic function Supports neuronal energy usage + plasticity; deficiency can worsen excitotoxic vulnerability R, G Supportive human + mechanistic Form/absorption variability; renal constraints for supplementation in some patients
21 NAD+ precursors (NR/NMN/NA/NAM) Restores NAD+ availability for redox + signaling NAMPT salvage; sirtuins; PARPs; CD38 Supports mitochondrial function; may improve resilience under oxidative/repair load R, G Animal > human (emerging) NAD “sinks” (CD38/PARP) can dominate; response varies by inflammation/age
22 Alpha-lipoic acid (ALA) Mitochondrial redox cofactor + antioxidant recycling PDH/α-KGDH cofactor; GSH recycling support Improves redox tone and mitochondrial efficiency (signals strongest in metabolic/oxidative phenotypes) R, G Small AD trials + mechanistic “Antioxidant” framing can be misleading—main value is mitochondrial/redox coupling support
23 Glutathione system support Detox + peroxide handling GSH, GPx, GR, NADPH supply (PPP) Reduces oxidative damage load that impairs mitochondria/synapses R, G Mechanistic GSH depends on substrates + NADPH; pushing one component may not fix system
24 Selenium (GPx capacity) Peroxide detox via selenoenzymes Glutathione peroxidases Supports antioxidant enzyme capacity (context-dependent) G Mixed human Narrower safety margin; avoid “more is better” mindset
31 CoQ10 (ubiquinone) ETC electron carrier (I/II→III) + membrane redox Complex I/II→III transfer Supports OXPHOS efficiency; may reduce electron leak under some conditions R, G Limited AD-specific Bioavailability/formulation matters; AD cognition data not robust
32 Cardiolipin / mitochondrial membranes (support axis) ETC supercomplex stability; cristae integrity Inner mitochondrial membrane architecture Membrane integrity affects ETC efficiency and ROS leak G Mechanistic Hard to “target” nutritionally in a clean way; effects indirect
33 Iron / copper homeostasis (burden control) Prevents metal-catalyzed oxidative damage Fenton chemistry burden; metal transport/storage Metal dyshomeostasis can amplify ROS and mitochondrial injury R, G Mechanistic + mixed human “Chelation” is not casually safe; needs careful framing and evidence
41 Ketone utilization (BHB/acetoacetate axis) Alternative brain fuel bypassing glucose bottlenecks MCT1/2 transport; ketolysis enzymes Addresses brain glucose hypometabolism by providing alternate substrate R, G Moderate (human MCI/AD signals exist) GI tolerance and adherence; response varies by genotype/metabolic status
42 Creatine / phosphocreatine shuttle ATP buffering and rapid energy stabilization Creatine kinase system May stabilize energy during stress; supports muscle/functional reserve that impacts cognition indirectly G Limited AD CNS benefit uncertain; stronger for muscle/functional outcomes
43 Acetyl-L-carnitine (ALCAR) Fatty acid oxidation support + acetyl group handling Carnitine shuttle; acetyl-CoA support May support mitochondrial energy and neuronal function (mixed clinical results) R, G Mixed human Benefits heterogeneous; not a universal cognitive improver
44 Medium-chain triglycerides (MCT oil → ketones) Rapid ketone support strategy Hepatic ketogenesis; brain ketone uptake Practical ketone-raising approach for some phenotypes R, G Moderate human GI effects; calorie load; titration matters
51 AMPK → PGC-1α biogenesis axis Mitochondrial number/quality regulation AMPK, PGC-1α, SIRT1 Supports long-term mitochondrial capacity and stress resistance G Mechanistic Most effects are slow; many “activators” are indirect and context-dependent
52 Mitophagy / autophagy quality control Removes damaged mitochondria PINK1/Parkin axis; autophagy machinery Damaged mitochondria drive ROS and energy failure; quality control is protective in theory G Mechanistic Autophagy modulation is double-edged; oversimplified “more autophagy = good” is risky
53 Exercise signaling (the “master cofactor”) Improves vascular + mitochondrial + neurotrophic tone BDNF; insulin sensitivity; AMPK/PGC-1α Most evidence-backed multi-pathway energy intervention for aging brain R, G Strong (human) Adherence/ability constraints; must be individualized
61 Cerebral perfusion / vascular health Fuel + oxygen delivery and waste clearance support Neurovascular unit; endothelial function Vascular dysfunction worsens hypometabolism and inflammation R, G Strong (human) Often upstream of “supplement” efficacy; if delivery is poor, cofactors underperform
62 Sleep / glymphatic clearance Waste clearance & metabolic recovery Glymphatic system; circadian regulation Supports clearance of metabolic byproducts; indirectly supports energy balance G Strong (human) Often neglected; impacts cognition and inflammation strongly
63 Oxygen utilization context (respiratory capacity) Oxidative metabolism support OXPHOS dependence If oxygen delivery/usage is limited, pushing mitochondrial cofactors won’t fully translate R, G Supportive More about system constraints than a “node to supplement”

TSF (Time-Scale Flag): P = 0–30 min, R = 30 min–3 hr, G = >3 hr (adaptation/phenotype). Evidence: "Strong (human)" = consistent clinical/epidemiologic support; "Moderate" = mixed but plausible human signals; "Emerging" = early-stage human; "Mechanistic" = preclinical/biochemical rationale.



Scientific Papers found: Click to Expand⟱
5663- BNL,    Osthole/borneol thermosensitive gel via intranasal administration enhances intracerebral bioavailability to improve cognitive impairment in APP/PS1 transgenic mice
- in-vivo, AD, NA
*ZO-1↓, *cl‑Casp3↓, *Bax:Bcl2↓, *MDA↓, *Apoptosis↓, *Aβ↓, *BACE↓, *cognitive↑, *BioAv↑, memory↑, P-gp↓, BioEnh↑,
5669- BNL,    Comparison of pharmacological activity and safety of different stereochemical configurations of borneol: L-borneol, D-borneol, and synthetic borneol
- Review, Nor, NA - Review, AD, NA - Review, Stroke, NA
*eff↑, *eff↑, *toxicity↝, *Inflam↓, *Bacteria↓, *neuroP↑, *Half-Life↝, *BBB↑, *BioEnh↑, *P-gp↓, *CYP3A4↓, *ROS↓, *neuroP↑,
3595- PI,    Black pepper and health claims: a comprehensive treatise
- Review, Var, NA - Review, AD, NA
*antiOx↑, *ROS↓, *chemoP↑, TumCG↓, *cognitive↑, *MMPs↓, *PGE2↓, *AP-1↓, *5LO↓, *COX1↓, *other↑, *other↑, *other↑, *SOD↑, *Catalase↑, *GSTs↑, *GSR↑, *other↑, *Weight↓, *BioEnh↑, *BioAv↑, *eff↑, *CYP3A2↓, *neuroP↑, *BP↓, *other↑,
3917- PS,    Phosphatidylserine, inflammation, and central nervous system diseases
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, *neuroP↑, *cognitive↑, *Choline↑, *IL1β↓, *IL6↓, *TNF-α↓, *Ach↑, *eff↑, *eff↑, *BioEnh↑, other↑,

Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Transcription & Epigenetics

other↑, 1,  

Proliferation, Differentiation & Cell State

TumCG↓, 1,  

Barriers & Transport

P-gp↓, 1,  

Drug Metabolism & Resistance

BioEnh↑, 1,  

Functional Outcomes

memory↑, 1,  
Total Targets: 5

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

antiOx↑, 1,   Catalase↑, 1,   GSR↑, 1,   GSTs↑, 1,   MDA↓, 1,   ROS↓, 2,   SOD↑, 1,  

Core Metabolism/Glycolysis

CYP3A2↓, 1,   CYP3A4↓, 1,  

Cell Death

Apoptosis↓, 1,   Bax:Bcl2↓, 1,   cl‑Casp3↓, 1,  

Transcription & Epigenetics

Ach↑, 1,   other↑, 5,  

Proliferation, Differentiation & Cell State

Choline↑, 1,  

Migration

5LO↓, 1,   AP-1↓, 1,   MMPs↓, 1,   ZO-1↓, 1,  

Barriers & Transport

BBB↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling

COX1↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 2,   PGE2↓, 1,   TNF-α↓, 1,  

Protein Aggregation

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance

BioAv↑, 2,   BioEnh↑, 3,   eff↑, 5,   Half-Life↝, 1,  

Clinical Biomarkers

BP↓, 1,   IL6↓, 1,  

Functional Outcomes

chemoP↑, 1,   cognitive↑, 3,   neuroP↑, 4,   toxicity↝, 1,   Weight↓, 1,  

Infection & Microbiome

Bacteria↓, 1,  
Total Targets: 41

Scientific Paper Hit Count for: BioEnh, bioenhancer
2 borneol
1 Piperine
1 Phosphatidylserine
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:38  Cells:%  prod#:%  Target#:1310  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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