Berberine / Akt Cancer Research Results

BBR, Berberine: Click to Expand ⟱
Features:

Berberine — Berberine is a protoberberine/isoquinoline alkaloid natural product found in plants such as Coptis, Berberis, and Phellodendron. It is a small-molecule phytochemical with pleiotropic metabolic, anti-inflammatory, and anticancer signaling effects rather than a single highly selective target profile. Its standard abbreviation is BBR. In oncology it is best classified as a multitarget natural-product lead compound and adjunct-sensitizer candidate, with strong preclinical evidence but no established standard anticancer regulatory use. Its translational profile is shaped by very low conventional oral bioavailability, extensive first-pass metabolism, broad tissue distribution, and substantial context dependence between cancer-cell pro-death effects and normal-cell cytoprotective redox effects.

Primary mechanisms (ranked):

  1. AMPK-centered metabolic stress with mitochondrial dysfunction, ATP depletion, and apoptosis/autophagy induction
  2. Suppression of aerobic glycolysis and hypoxia signaling, including HIF-1α, GLUT1, HK2, LDHA, and PKM2-linked tumor metabolism
  3. Anti-proliferative cell-cycle control with cyclin/CDK suppression and tumor suppressor reactivation
  4. Inhibition of PI3K/AKT, MAPK/ERK, JAK/STAT, and NF-κB inflammatory-survival signaling
  5. Anti-metastatic and anti-EMT activity via Wnt/β-catenin, TGF-β/Smad, FAK/RhoA/ROCK, MMPs, and CXCR4-related programs
  6. Pro-oxidant mitochondrial ROS elevation and ER-stress/caspase signaling in many cancer models, with opposite antioxidant/NRF2-supportive effects in some normal-cell and non-cancer settings
  7. Context-dependent chemosensitization and radiosensitization, including effects on hypoxia signaling and DNA-repair competence
  8. Emerging ferroptosis-related activity in some tumor models, but not a universal dominant mechanism across berberine biology

Bioavailability / PK relevance: Conventional oral berberine has poor systemic bioavailability, often cited as below 1% in animal studies, because of limited absorption, P-glycoprotein efflux, first-pass intestinal/hepatic metabolism, and self-aggregation. Human exposure is usually in the low ng/mL plasma range with conventional dosing, while multiple metabolites may contribute to activity. Tissue distribution can exceed plasma levels, but PK remains a major clinical translation constraint.

In-vitro vs systemic exposure relevance: Many anticancer in-vitro studies use roughly 10–100 µM, commonly around 20–50 µM, which usually exceeds readily achievable conventional plasma exposure after standard oral dosing. Therefore, direct translation of cell-culture potency to systemic monotherapy expectations is limited unless local gut exposure, tissue accumulation, metabolite contribution, formulation enhancement, or combination use is specifically relevant.

Clinical evidence status: Strong preclinical and mechanistic evidence; limited early human oncology/chemoprevention evidence; no established phase III anticancer efficacy standard and no mainstream regulatory approval as an anticancer drug. Current clinical relevance is best viewed as investigational and adjunct-oriented rather than proven standalone oncology therapy.

Berberine is a chemical found in some plants like European barberry, goldenseal, goldthread, Oregon grape, phellodendron, and tree turmeric. Berberine is a bitter-tasting and yellow-colored chemical.
Coptis (commonly referring to Coptidis Rhizoma, a traditional Chinese medicinal herb) contains bioactive alkaloids (most notably berberine and coptisine) that have been studied for their pharmacological effects—including their influence on reactive oxygen species (ROS) and related pathways.

– Berberine is known for its relatively low oral bioavailability, often cited at less than 1%. This low bioavailability is mainly due to poor intestinal absorption and active efflux by transport proteins such as P-glycoprotein.
– Despite the low bioavailability, berberine is still pharmacologically active, and its metabolites may also contribute to its overall effects.

• Effective Dosage in Studies
– Many clinical trials or preclinical studies use dosages in the range of 500 to 1500 mg per day, typically administered in divided doses.
– Therefore, to obtain a bioactive dose of berberine, supplementation in a standardized extract form is necessary.

-IC50 in cancer cell lines: Approximately 10–100 µM (commonly around 20–50 µM in many models)
-IC50 in normal cell lines: Generally higher (often above 100 µM), although this can vary with cell type
- In vivo studies: Dosing regimens in animal models generally range from about 50 to 200 mg/kg
- very effective AChE inhibitor (Alzheimers)
- Berberine may enhance the effects of blood-thinning medications like warfarin and aspirin.


-Note half-life reports vary 2.5-90hrs?.
-low solubility of apigenin in water : 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 : , MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, EZH2↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, Hh↓, GLi1↓, CD133↓, β-catenin↓, n-myc↓, sox2↓, notch2↓, nestin↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, α↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Rank Pathway / Target Axis Direction Primary Effect Notes / Cancer Relevance Ref
1 AMPK → mTOR axis ↑ AMPK / ↓ mTOR signaling Metabolic stress + growth suppression In vivo/in vitro colon tumorigenesis model: berberine activates AMPK, inhibits mTOR signaling and reduces proliferation/tumorigenesis, growth suppression, autophagy, HIF-1α ↓, glycolysis ↓, berberine’s known mitochondrial/energetic effects (ref)
2 Mitochondrial dysfunction / ROS generation ↑ ROS / mitochondrial stress Upstream metabolic trigger Berberine inhibits mitochondrial function, increases ROS, and contributes to AMPK activation and downstream apoptosis (ref)
3 Mitochondrial apoptosis (cytochrome c release) ↑ cytochrome c release Intrinsic death signaling Oral cancer model: berberine reduces mitochondrial membrane potential, releases cytochrome c, activates caspase-3 (ref)
4 Intrinsic apoptosis (caspase-3 activation) ↑ caspase-3 activation Programmed cell death Same oral cancer study documents caspase-3 activation as a key execution marker (ref)
5 NF-κB signaling (p65 activation) ↓ NF-κB activation Reduced pro-survival transcription Colon cancer model reports inhibition of p65 phosphorylation; interpreted as secondary to metabolic/redox stress (ref)
6 Cell cycle control ↑ G1 arrest Proliferation blockade Prostate cancer model: berberine induces G1-phase cell cycle arrest and caspase-3–dependent apoptosis (ref)
7 Hypoxia / glycolysis signaling (HIF-1α) ↓ HIF-1α protein Warburg / glycolysis suppression Berberine suppresses mTOR and reduces HIF-1α protein expression downstream of AMPK activation (ref)
8 Angiogenesis signaling (HIF-1α → VEGF axis) ↓ VEGF signaling Reduced vascular support Lung cancer study: berberine suppresses VEGF signaling alongside HIF-1α inhibition (ref)
9 PI3K–AKT–mTOR signaling ↓ PI3K / AKT / mTOR Survival pathway suppression Gastric cancer paper: berberine represses PI3K/AKT/mTOR signaling and improves chemosensitivity (ref)
10 Migration / invasion programs ↓ migration & invasion Anti-metastatic phenotype Tongue SCC model: berberine suppresses migration and invasion with associated signaling changes (ref)
11 Telomerase (hTERT) / immortalization axis ↓ hTERT-related signaling Reduced proliferative capacity Lung cancer study includes AP-2/hTERT regulatory axis modulation by berberine (ref)
12 In vivo tumor suppression ↓ tumorigenesis Demonstrated anti-tumor effect Colon tumorigenesis model confirms reduced proliferation and tumor burden with berberine (ref)


Akt, PKB-Protein kinase B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes; Akt2 is an important signaling molecule in the insulin signaling pathway. It is required to induce glucose transport.

Inhibitors:
-Curcumin: downregulate AKT phosphorylation and signaling.
-Resveratrol
-Quercetin: inhibit the PI3K/AKT pathway.
-Epigallocatechin Gallate (EGCG)
-Luteolin and Apigenin: inhibit AKT phosphorylation


Scientific Papers found: Click to Expand⟱
2707- BBR,    Berberine exerts its antineoplastic effects by reversing the Warburg effect via downregulation of the Akt/mTOR/GLUT1 signaling pathway
- in-vitro, Liver, HepG2 - in-vitro, BC, MCF-7
GLUT1↓, Akt↓, mTOR↓, ATP↓, GlucoseCon↓, TumCP↓, Warburg↓, selectivity↑, TumCCA↑, Glycolysis↓,
2698- BBR,    A gene expression signature-based approach reveals the mechanisms of action of the Chinese herbal medicine berberine
- Analysis, BC, MDA-MB-231
HDAC↓, Akt↓, mTOR↓, ER Stress↑, TumAuto↑, AMPK↑, mTOR∅, HDAC∅, ac‑α-tubulin↑,
2686- BBR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Nor, NA
Inflam↓, IL6↓, MCP1↓, COX2↓, PGE2↓, MMP2↓, MMP9↓, DNAdam↑, eff↝, Telomerase↓, Bcl-2↓, AMPK↑, ROS↑, MMP↓, ATP↓, p‑mTORC1↓, p‑S6K↓, ERK↓, PI3K↓, PTEN↑, Akt↓, Raf↓, MEK↓, Dose↓, Dose↑, selectivity↑, TumCCA↑, eff↑, EGFR↓, Glycolysis↓, Dose?, p27↑, CDK2↓, CDK4↓, cycD1/CCND1↓, cycE/CCNE↓, Bax:Bcl2↑, Casp3↑, Casp9↑, VEGFR2↓, ChemoSen↑, eff↑, eff↑, PGE2↓, JAK2↓, STAT3↓, CXCR4↓, CCR7↓, uPA↓, CSCs↓, EMT↓, Diff↓, CD133↓, Nestin↓, n-MYC↓, NOTCH↓, SOX2↓, Hif1a↓, VEGF↓, RadioS↑,
5181- BBR,  Cisplatin,    Berberine Improves Chemo-Sensitivity to Cisplatin by Enhancing Cell Apoptosis and Repressing PI3K/AKT/mTOR Signaling Pathway in Gastric Cancer
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
tumCV↓, MDR1↓, ChemoSen↑, PI3K↓, Akt↓, mTOR↓,
5180- BBR,    Berberine Targets AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth
- in-vitro, NSCLC, NA
TumCMig↓, TumCP↓, Apoptosis↑, TFAP2A↓, hTERT/TERT↓, NF-kB↓, COX2↓, Hif1a↓, VEGF↓, Akt↓, p‑ERK↓, Cyt‑c↑, cl‑Casp↑, cl‑PARP↑, PI3K↓, Akt↓, Raf↓, MEK↓, ERK↓,
4298- BBR,    Berberine mitigates cognitive decline in an Alzheimer’s Disease Mouse Model by targeting both tau hyperphosphorylation and autophagic clearance
- in-vivo, AD, NA
*cognitive↑, *p‑tau↓, *GSK‐3β↓, *PP2A↑, *memory↑, *Akt↑, *LC3II↑, *Beclin-1↑,
3684- BBR,    Neuroprotective effects of berberine in animal models of Alzheimer’s disease: a systematic review of pre-clinical studies
- Review, AD, NA
*Inflam↓, *antiOx↓, *AChE↓, *BChE↓, *MAOA↓, *MAOB↓, *lipid-P↓, *GSH↑, *ROS↓, *APP↓, *BACE↓, *p‑tau↓, *NF-kB↓, *TNF-α↓, *IL1β↓, *MAPK↓, *PI3K↓, *Akt↓, *neuroP↑, *memory↑,
3681- BBR,    The efficacy and mechanism of berberine in improving aging-related cognitive dysfunction: A study based on network pharmacology
- in-vivo, AD, NA
*memory↑, *cognitive↑, MAPK↑, *Akt↑, *PI3K↑, *TP53↑, *Jun↓, *HSP90↑, *neuroP↑, *Inflam↓, *antiOx↑, *p16↓, *ER Stress↓,
3680- BBR,    Network pharmacology reveals that Berberine may function against Alzheimer’s disease via the AKT signaling pathway
- in-vivo, AD, NA
*Akt↑, *neuroP↑, *p‑ERK↑, *Aβ↓, *Inflam↓, *ROS↓, *BioAv↑, *BBB↑, *Half-Life↝, *memory↑, *cognitive↑, *HSP90↑, *APP↓, *mTOR↓, *P70S6K↓, *CD31↑, *VEGF↑, *N-cadherin↑, *Apoptosis↓,
3678- BBR,    Network pharmacology study on the mechanism of berberine in Alzheimer’s disease model
- Review, AD, NA
*APP↓, *PPARγ↑, *NF-kB↓, *Aβ↓, *cognitive↑, *antiOx↑, *Inflam↓, *Apoptosis↓, *BioAv↑, *BioAv↝, *BBB↑, *motorD↑, *NRF2↑, *HO-1↑, *ROS↓, *p‑Akt↑, *p‑ERK↑,
1387- BBR,    Antitumor Activity of Berberine by Activating Autophagy and Apoptosis in CAL-62 and BHT-101 Anaplastic Thyroid Carcinoma Cell Lines
- in-vitro, Thyroid, CAL-62
TumCG↓, Apoptosis↑, LC3B↑, ROS↑, PI3K↓, Akt↓, mTOR↓,
1299- BBR,    Effects of Berberine and Its Derivatives on Cancer: A Systems Pharmacology Review
- Review, NA, NA
TumCCA↑, TP53↑, COX2↓, Bax:Bcl2↑, ROS↑, VEGFR2↓, Akt↓, ERK↓, MMP2↓, MMP9↓, IL8↑, P21↑, p27↑, E-cadherin↓, Fibronectin↓, cMyc↓,
1102- BBR,    Berberine suppressed epithelial mesenchymal transition through cross-talk regulation of PI3K/AKT and RARα/RARβ in melanoma cells
- in-vitro, Melanoma, B16-BL6
TumCMig↓, TumCI↓, EMT↓, p‑PI3K↓, p‑Akt↓, RARα↓, RARβ↑, RARγ↑, E-cadherin↑, N-cadherin↓,
2682- BBR,    Berberine Inhibited Growth and Migration of Human Colon Cancer Cell Lines by Increasing Phosphatase and Tensin and Inhibiting Aquaporins 1, 3 and 5 Expressions
- in-vitro, CRC, HT29 - in-vitro, CRC, SW480 - in-vitro, CRC, HCT116
TumCP↓, TumCMig↓, TumCI↓, Apoptosis↑, necrosis↑, AQPs↓, PTEN↑, PI3K↓, Akt↓, p‑Akt↓, mTOR↓, p‑mTOR↓,
2670- BBR,    Berberine: A Review of its Pharmacokinetics Properties and Therapeutic Potentials in Diverse Vascular Diseases
- Review, Var, NA
*Inflam↓, *antiOx↑, *Ca+2↓, *BioAv↓, *BioAv↑, *BioAv↑, *angioG↑, *MAPK↓, *AMPK↓, *NF-kB↓, VEGF↓, PI3K↓, Akt↓, MMP2↓, Bcl-2↓, ERK↓,
2021- BBR,    Berberine: An Important Emphasis on Its Anticancer Effects through Modulation of Various Cell Signaling Pathways
- Review, NA, NA
*antiOx?, *Inflam↓, Apoptosis↑, TumCCA↑, BAX↑, eff↑, VEGF↓, PI3K↓, Akt↓, mTOR↓, Telomerase↓, β-catenin/ZEB1↓, Wnt↓, EGFR↓, AP-1↓, NF-kB↓, COX2↑, NRF2↓, RadioS↑, STAT3↓, ERK↓, AR↓, ROS↑, eff↑, selectivity↑, selectivity↑, BioAv↓, DNMT1↓, cMyc↓,

Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↓, 1,   ROS↑, 4,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   MEK↓, 2,   MMP↓, 1,   Raf↓, 2,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2,   cMyc↓, 2,   GlucoseCon↓, 1,   Glycolysis↓, 2,   RARα↓, 1,   RARβ↑, 1,   RARγ↑, 1,   p‑S6K↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 11,   p‑Akt↓, 2,   Apoptosis↑, 4,   BAX↑, 1,   Bax:Bcl2↑, 2,   Bcl-2↓, 2,   cl‑Casp↑, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   hTERT/TERT↓, 1,   MAPK↑, 1,   necrosis↑, 1,   p27↑, 2,   Telomerase↓, 2,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   cl‑PARP↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   TFAP2A↓, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CSCs↓, 1,   Diff↓, 1,   EMT↓, 2,   ERK↓, 5,   p‑ERK↓, 1,   HDAC↓, 1,   HDAC∅, 1,   mTOR↓, 6,   mTOR∅, 1,   p‑mTOR↓, 1,   p‑mTORC1↓, 1,   n-MYC↓, 1,   Nestin↓, 1,   NOTCH↓, 1,   PI3K↓, 7,   p‑PI3K↓, 1,   PTEN↑, 2,   SOX2↓, 1,   STAT3↓, 2,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

AP-1↓, 1,   E-cadherin↓, 1,   E-cadherin↑, 1,   Fibronectin↓, 1,   MMP2↓, 3,   MMP9↓, 2,   N-cadherin↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 3,   uPA↓, 1,   ac‑α-tubulin↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 2,   Hif1a↓, 2,   VEGF↓, 4,   VEGFR2↓, 2,  

Barriers & Transport ⓘ

AQPs↓, 1,   GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

CCR7↓, 1,   COX2↓, 3,   COX2↑, 1,   CXCR4↓, 1,   IL6↓, 1,   IL8↑, 1,   Inflam↓, 1,   JAK2↓, 1,   MCP1↓, 1,   NF-kB↓, 2,   PGE2↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 2,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   eff↑, 5,   eff↝, 1,   MDR1↓, 1,   RadioS↑, 2,   selectivity↑, 4,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 2,   hTERT/TERT↓, 1,   IL6↓, 1,   TP53↑, 1,  
Total Targets: 113

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx?, 1,   antiOx↓, 1,   antiOx↑, 3,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   NRF2↑, 1,   ROS↓, 3,  

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Akt↑, 3,   p‑Akt↑, 1,   Apoptosis↓, 2,   MAPK↓, 2,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   HSP90↑, 2,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

p16↓, 1,   TP53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 2,   GSK‐3β↓, 1,   Jun↓, 1,   mTOR↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   PI3K↑, 1,  

Migration ⓘ

APP↓, 3,   Ca+2↓, 1,   CD31↑, 1,   N-cadherin↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   VEGF↑, 1,  

Barriers & Transport ⓘ

BBB↑, 2,  

Immune & Inflammatory Signaling ⓘ

IL1β↓, 1,   Inflam↓, 6,   NF-kB↓, 3,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   BChE↓, 1,   MAOA↓, 1,   p‑tau↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 2,   BACE↓, 1,   MAOB↓, 1,   PP2A↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 4,   BioAv↝, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

TP53↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 4,   memory↑, 4,   motorD↑, 1,   neuroP↑, 3,  
Total Targets: 56

Scientific Paper Hit Count for: Akt, PKB-Protein kinase B
16 Berberine
1 Cisplatin
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#:41  Target#:4  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

Home Page