BBB Cancer Research Results

BBB, Blood-Brain Barrier Permeability: Click to Expand ⟱
Source:
Type:
Blood-Brain Barrier(BBB) is a term often used regarding if a product has the ability to cross the BBB.
Scientific Papers found: Click to Expand⟱
4291- EGCG,    Structure-based discovery of small molecules that disaggregate Alzheimer’s disease tissue derived tau fibrils in vitro
- in-vitro, AD, NA
*tau↓, EGCG, abundant in green tea, has long been known to disaggregate tau and other amyloid fibrils, but EGCG has poor drug-like properties, failing to fully penetrate the brain.
*BBB∅, EGCG itself is a poor therapeutic candidate owing to its polyphenolic molecular structure, which results in unfavorable drug-like properties and restricts brain penetration.

7026- Fuc,    Fucoidan
- Review, AD, NA
*Inflam↓, May reduce immune cell mediated inflammation and oxidative stress, but has very low oral bioavailability.
*ROS↓,
*BioAv↓,
*GutMicro↑, May exert beneficial effects through modulation of the intestine/microbiome
*neuroP↑, Neuroprotective Benefit: Can protect against onset of inflammatory and oxidative damage by mitigating immune cell activation in animal models.
*glucose↝, May help regulate glucose homeostasis, have anti-thrombotic effects, and improve tolerability of chemotherapy, but benefits are limited by poor oral bioavailability.
*AntiThr↑,
*chemoP↑,
*Half-Life↝, Half-life: Varies with preparation (~1-3 hours in rats)
*BBB∅, BBB: Not penetrant
*AntiAge↑, Diets rich in fucoidan associated with increased lifespan and lower cancer incidence.
Risk↑,

8039- IVM,    Ivermectin-Induced Apoptotic Cell Death in Human SH-SY5Y Cells Involves the Activation of Oxidative Stress and Mitochondrial Pathway and Akt/mTOR-Pathway-Mediated Autophagy
- NA, neuroblastoma, SH-SY5Y
*toxicity↑, Ivermectin (IVM) could cause potential neurotoxicity; however, the precise molecular mechanisms remain unclear.
TumCD↑, The results show that IVM treatment (2.5–15 μM) for 24 h could induce dose-dependent cell death in SH-SY5Y cells.
ROS↑, Compared to the control, IVM treatment significantly promoted the production of ROS, mitochondrial dysfunction, and cell apoptosis.
mtDam↑,
Apoptosis↑,
MitoP↑, IVM treatment also promoted mitophagy and autophagy, which were charactered by the decreased expression of phosphorylation (p)-Akt and p-mTOR proteins, increased expression of LC3II, Beclin1, ATG5, PINK, and Pakin1 proteins and autophagosome formatio
TumAuto↑,
p‑Akt↓,
p‑mTOR↓,
LC3II↑,
Beclin-1/ATG6↑,
ATG5↑,
PINK1↑,
PARK2↑,
tumCV↓, At 6 h and 12 h, IVM treatment at 15 μM significantly decreased the cell viabilities to 44.3% and 35.6% (both p < 0.01), respectively;
MDA↑, IVM treatment at the doses of 10 and 15 μM significantly increased the levels of MDA to 0.25 nmol/mg and 0.76 nmol/mg protein (both p < 0.01) (Figure 3B), respectively; increased the activities of SOD to 1.61 U/mg and 3.48 U/mg protein (both p < 0.
SOD↑,
Catalase↑,
eff↓, NAC treatment at 10 mM significantly inhibited the IVM-induced production of ROS
MMP↓, IVM treatment significantly decreased the ΔΨm in a dose-dependent manner.
BAX↑, IVM treatment significantly increased the expressions of Bax, cleaved caspase-3, cleaved caspase-9, cleaved PARP-1 proteins, and CytC proteins, and decreased the expressions of Bcl-2 and pro-caspase-3 proteins.
cl‑Casp3↑,
cl‑Casp9↑,
cl‑PARP↑,
Cyt‑c↑,
Bcl-2↓,
proCasp3↓,
Bax:Bcl2↑, IVM treatment at 10 μM significantly increased the ratio of Bax/Bcl-2 to 2.6-fold
eff↑, Inhibition of Autophagy Improves Ivermectin-Induced Cytotoxicity, Oxidative Stress, and Apoptotic Cell Death
*AntiP↑, IVM has been widely used as an antiparasitic drug in human and veterinary medicines
*Inflam↓, IVM exhibited several new threptic effects, including anti-cancer, anti-inflammation, anti-diabetic, and antiviral effects
*AntiDiabetic↑,
*AntiViral↑,
BBB∅, In relation to the current recommended dose, IVM is not thought to readily cross the blood–brain barrier in humans
toxicity↝, It has been reported that an IVM overdose could induce neurotoxicity in SARS-CoV-2 patients and the main neurotoxic symptoms include confusion, ataxia, weakness, hypotension, and seizures

8029- IVM,    Ivermectin in Cancer Treatment: Should Healthcare Providers Caution or Explore Its Therapeutic Potential?
- Review, Var, NA
TumCP↓, Ivermectin's anticancer effects, including inhibition of cancer cell proliferation, induction of apoptosis, and modulation of signaling pathways (e.g., Wnt/β-catenin, Akt/mTOR) across various cancers.
Apoptosis↑,
Wnt↓,
β-catenin/ZEB1↓,
Akt↓, Ivermectin inhibited the Akt/mTOR pathway, a key regulator of tumor growth and metabolism
mTOR↓,
BBB∅, exhibiting minimal toxicity to humans due to poor penetration of the blood–brain barrier
ROS↑, In colorectal cancer, it induces reactive oxygen species (ROS)-mediated mitochondrial apoptosis by disrupting mitochondrial membrane potential, activating caspases (e.g., caspase-3/9
MMP↓,
Casp3↓,
Casp9↑,
TumCCA↑, Ivermectin induced caspase-dependent apoptosis and G0/G1-phase cell cycle arrest, partly through increased p53 expression in cells with wild-type p53, promoting cell death
P53↑,
cMyc↓, downstream genes like c-Myc and MMP-9 [
MMP9↓,
HSP27↓, inhibits HSP27, which is synergistically lethal to cells with oncogenic activation of EGFR o
ICD↑, induces immunogenic cancer cell death (ICD) and robust T-cell infiltration
eff↑, synergizes with anti-PD1 antibody to control tumor growth and induce protective immunity
*AntiP↑, Ivermectin has become a cornerstone therapy for treating human parasitic diseases like onchocerciasis and strongyloidiasis.


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:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   ICD↑, 1,   MDA↑, 1,   PARK2↑, 1,   ROS↑, 2,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 2,   mtDam↑, 1,   PINK1↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp3↓, 1,   cl‑Casp3↑, 1,   proCasp3↓, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP27↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3II↑, 1,   MitoP↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

mTOR↓, 1,   p‑mTOR↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

MMP9↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB∅, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↓, 1,   eff↑, 2,  

Functional Outcomes(tgid=23) ⓘ

Risk↑, 1,   toxicity↝, 1,  
Total Targets: 44

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiP↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↝, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB∅, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

tau↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,   AntiDiabetic↑, 1,   chemoP↑, 1,   neuroP↑, 1,   toxicity↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,  
Total Targets: 16

Scientific Paper Hit Count for: BBB, Blood-Brain Barrier Permeability
2 Ivermectin
1 EGCG (Epigallocatechin Gallate)
1 Fucoidan
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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