Dose Cancer Research Results
Dose, Dosage: Click to Expand ⟱
| Source: |
| Type: |
Drug dosage vs efficacy, and actual dosage number of research papers.
|
Scientific Papers found: Click to Expand⟱
Dose⇅, At high concentrations (20–40 μM), AXT triggered apoptosis in U251-MG cells, as it has been previously shown in other cancer cell lines. However, low concentrations (4–8 μM) of AXT were found to upregulate the proliferative cell cycle.
ROS∅, low concentrations, AXT did not affect the intracellular ROS levels, while the superoxide dismutase activity increased moderately.
SOD↑,
CDK1↑, Low Dose Astaxanthin Treatments Trigger the Hormesis of Human Astroglioma Cells by Up-Regulating the Cyclin-Dependent Kinase and Down-Regulated the Tumor Suppressor Protein P53
P53↓,
TumCP⇅, we found that U251-MG cells show a biphasic response to AXT, that is low doses of AXT have a proliferative effect, with a maximum survival increase of 130.4 ± 2.4% after treatment with 5 µM of AXT, while AXT concentrations over 20 µM have an apoptoti
ROS↑, Treatment with High AXT Concentrations Increased Intracellular ROS Levels while Low AXT Concentrations did not Affect ROS Levels
Apoptosis↑, Celecoxib induced apoptosis independent of COX-2 activity.
Casp8↑, This event accompanied the activation of caspase-8 and -9 with Bid cleavage and the loss of mitochondrial membrane potential.
Casp9↑,
cl‑BID↑,
MMP↓,
NF-kB↑, Celecoxib-induced apoptosis is associated with NF-κB activation.
Dose⇅, The chemopreventive effect of celecoxib was also achieved only at relatively high doses (400–800 mg daily) in a human clinical trial, but not at a therapeutic daily dose of 200 mg
chemoPv⇅,
COX2↓, less than 10 μM of celecoxib is needed to inhibit the COX activity, while the concentrations required to inhibit tumor cell growth range from 30 μM to 100 μM
| - |
Review, |
Arthritis, |
NA |
|
|
|
- |
Review, |
IBD, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Park, |
NA |
|
|
|
*other↝, The most abundant and promising bioactive compound derived from the root of this plant is celastrol, also called tripterine, which possess a broad range of biological activities
*other↝, TW is generally used in the treatment of Crohn’s disease (CD) in China.
*CRP↓, Inflammatory parameters, including c-reactive protein (CRP), also decreased
*eff↝, Etanercept plus TW had an equivalent therapeutic effect to that of Etanercept plus MTX and were both well tolerated
*other↑, TW in human kidney transplantation (26). Rejection occurred in 4.1% of patients treated with TW versus 24.5% of control patients, showing efficacy in the prevention of renal allograph rejection
*CXCR4↓, celastrol decreases hypoxia-induced FLS invasion by inhibiting HIF-1α-mediated CXCR4 transcription
*IL1β↓, Authors have shown that it decreases the production of IL-1β, IL-6, IL-17, IL-18, and TNF by SIC cells harvested from arthritic rats
*IL6↓,
*IL17↓,
*IL18↓,
*TNF-α↓,
*MMP9↓, celastrol reduces MMP-9 production, which limits bone damage
*PGE2↓, celastrol suppresses LPS-induced expression of PEG2 via the downregulation of COX-1 and COX-2 activation
*COX1↓,
*COX2↓,
*PI3K↓, associated with a decrease in PI3K/Akt pathway
*Akt↓,
*other↑, Remarkably, this bone-protective property of celastrol in arthritic models is further supported by studies performed in cancer models
TumCCA↑, celastrol induces cell cycle arrest, apoptosis, and autophagy by the activation of reactive oxygen species (ROS)/c-Jun N-terminal kinases (JNK) signaling pathway
Apoptosis↑,
ROS↑,
JNK↑,
TumAuto↑, celastrol is still able to induce autophagy through HIF/BNIP3 activation
Hif1a↓, The inhibitory effect of celastrol on angiogenesis is mediated by the suppression of HIF-1α,
BNIP3↝,
HSP90↓, The inhibition of HSP90 by celastrol
Fas↑, activation of Fas/Fas ligand pathway in non-small-cell lung cancer
FasL↑,
ETC↓, inhibition of mitochondrial respiratory chain (MRC) complex I
VEGF↓, This inhibition of HIF-1α leads to the decrease of its target genes, such as the VEGF
angioG↓, Angiogenesis Inhibition
RadioS↑, celastrol can overcome tumor resistance to radiotherapy in prostate (129) and lung cancer cells
*neuroP↑, celastrol is a promising neuroprotective agent in animal models of neurodegenerative diseases, such as Parkinson disease (149), Huntington disease (149–151), Alzheimer disease
*HSP70/HSPA5↑, his induction of HSP70 by celastrol explains its beneficial effects not only in neurodegenerative disorders but also in inflammatory diseases.
*ROS↓, celastrol protects human dopaminergic cells from injury and apoptosis and prevents ROS generation and mitochondrial membrane potential loss
*MMP↑,
*Cyt‑c↓, It inhibits cytochrome c release, Bax/Bcl-2 alterations, caspase-9/3 activation, and p38 MAPK activation
*Casp3↓,
*Casp9↓,
*MAPK↓,
*Dose⇅, Authors discuss that it seems to have a narrow therapeutic window, and suggest that it may have a biphasic effect with protective properties at low concentrations and toxic effects at higher concentrations.
*HSPs↑, induces a set of HSPs (HSP27, 32, and 70) in rat cerebral cortical cultures, which are selectively impacted during the progression of this disease
BioAv↓, Due to this poor water solubility, celastrol has low bioavailability. oral administration of celastrol in rats results in ineffective absorption into the systemic circulation, with an absolute bioavailability of 17.06%
Dose↝, narrow therapeutic window of dose together with the occurrence of adverse effects. Our own data showed in vivo that the doses of 2.5 and 5 μg/g/day are effective and non-toxic in the treatment of arthritis in rats;
*toxicity↝, Our previous studies have already demonstrated that a high dose of the honokiol microemulsion (0.6 μg/mL) induces developmental toxicity in rats and zebrafish by inducing oxidative stress.
*ROS↓, In zebrafish, low doses of honokiol microemulsion (0.15, 0.21 μg/mL) significantly decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) and increased the mRNA expression of bcl-2.
*ROS↑, In contrast, high dose (0.6 μg/mL) increased the levels of ROS and MDA, decreased activities and mRNA expression of superoxide dismutase (SOD) and catalase (CAT), and increased mRNA expression of bax, c-jnk, p53 and bim.
*Dose⇅, In rat pheochromocytoma cells (PC12 cells), low doses of the honokiol microemulsion (1, 5, 10 µM) exerted a protective effect against H2O2-induced oxidative damage while high doses (≥20 µM) induced oxidative stress, which further confirms the dual ef
*BioAv↑, highly lipophilic property of honokiol allows it to readily cross the blood-brain barrier and blood-cerebrospinal fluid barrier with high bioavailability.
*BioAv↓, However, this property also limits its clinical usage due to low oral bioavailability and difficulty in intravenous administration.
*ROS⇅, levels of ROS and MDA were significantly decreased at a concentration of 0.21 μg/mL and increased at a concentration of 0.6 μg/mL in both 24 and 96 hpf embryos
*SOD↓, The activity of SOD showed only a slight reduction at 20 µM but was significantly reduced at 40 and 80 μM
*toxicity↑, According to the human rat equivalent dosage conversion, the potential toxic dose in humans may be 320 µg/kg/d
ANXA7↑, Exposure to EECP significantly increased ANXA7 expression and ROS level
ROS↑,
NF-kB↓, NF-κB p65 level and mitochondrial membrane potential were depressed by EECP dramatically.
MMP↓,
selectivity↑, Interestingly, EECP had little or small cytotoxicity on normal human umbilical vein endothelial cells (HUVECs)
Dose⇅, propolis plays a dual role on ROS depending on concentrations: at high concentration, it exerts a prooxidant effect; at low concentration, it can also act as an antioxidant by scavenging free radicals.
ROS⇅,
tumCV↓, PEITC dose-dependently inhibited the viability of K7M2 murine osteosarcoma cells with an IC50 value of 33.49 μM at 24 h.
TumCP↓, PEITC (1, 15, 30 μM) dose-dependently inhibited the cell proliferation, caused G2/M cell cycle arrest, depleted glutathione (GSH), generated reactive oxygen species (ROS)
TumCCA↑,
GSH↓,
ROS↑,
Ferroptosis↑, altered iron metabolism, and triggered multiple forms of cell death, namely ferroptosis, apoptosis, and autophagy in K7M2 cells.
Apoptosis↑,
TumAuto↑,
MAPK↑, PEITC treatment activated MAPK signaling pathway, and ROS generation was a major cause of PEITC-induced cell death.
TumCG↓, osteosarcoma mouse model, administration of PEITC (30, 60 mg/kg every day, ig, for 24 days) significantly inhibited the tumor growth
Dose⇅, but higher dose of PEITC (90 mg/kg every day) compromised its anti-osteosarcoma effect.
*ROS↓, liver is the depot for most selenoproteins, which can reduce oxidative stress, inhibit tumor growth, and prevent other liver damage.
*hepatoP↑, their hepatoprotective properties
*selenoP↑,
*ALAT↓, (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (AP). However, the introduction of SeNPs significantly reduced the change in the level of these enzymes
*AST↓,
*GSH↑, significant increase in the content of glutathione and glutathione peroxidase in the liver
*GPx↑,
*TNF-α↓, In addition, the expression level of TNF-α, IL-6, NF-kB, and p65 genes was significantly increased in the cadmium-treated group (compared with the control), co-treatment of SeNPs and lacto-SeNPs led to a decrease in the expression of these genes.
*IL6↓,
*NF-kB↓,
*p65↓,
*Dose⇅, lactobacilli were used to restore Se from sodium selenite, while the synthesized nanoparticles had a size of 42.4 ± 10.5 nm and a zeta potential of −36.6 mV.
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
TumAuto↑, Spermidine has dual effects on cancers by targeting oncogenes, immunity, autophagy or apoptosis.
Apoptosis↑,
OS↑, Dietary spermidine intake has association with prolonged survival of cancer patients at the early stage.
CRM↑, increased uptake of spermidine as a caloric restriction mimic can reduce overall mortality associated with cancers.
TumCG⇅, Increased intake of polyamine seems to suppress tumorigenesis, but appears to accelerate the growth of established tumors.
cardioP↑, spermidine can protect from pathological events including two major death causes: cardiovascular disease (CVD) and cancer [15]
cognitive↑, and other aging-related diseases such as cognitive impairment during Alzheimer’s disease (AD) and Parkinson’s disease (PD)
*Dose⇅, spermidine at too high level could be detrimental to patients suffering from cancer, aging, innate immunity and cognitive impairment during AD and PD
ChemoSen↑, Supplementing chemotherapy and radiotherapy with selenium has been shown to have benefits against various cancers.
radioP↑,
QoL↑, This approach has also been shown to alleviate the side effects associated with standard cancer therapies and improve the quality of life in patients.
Risk↓, selenium levels in patients have been correlated with various cancers
*selenoP↑, Selenium is present in all mammals and is utilized by selenoproteins
TumCP↓, It has been reported that Se possesses anti-proliferative, anti-inflammatory, and anti-viral activities in addition to immune altering properties and has been implicated in various cancers
Inflam↓,
ChemoSen↑, Selenium-based compounds exhibit chemopreventive or chemotherapeutic properties through regulation of various processes such as cell cycle arrest, apoptosis, angiogenesis, etc.
TumCCA↑,
Apoptosis↑,
angioG↓,
Dose⇅, The amount of the selenium agent administered can influence whether prooxidant or antioxidant activity is observed.
ROS↑, Selenium-based compounds have been shown to exhibit chemopreventive and anticancer properties through prooxidant activities and the regulation of cellular redox homeostasis by altering thiol groups in multiple metabolic pathways, stimulating the prod
eff↑, The potency of selenium in an in vitro model of lung adenocarcinoma was increased with the addition of fish oil
Risk↓, In clinical trials, it has been observed that selenium and vitamin C supplementation decrease the incidence and mortality of gastric and lung cancer
eff∅, A selenium supplementation did not negatively impact the efficacy of chemotherapy
CSCs↓, Selenium Is Potent in Leukemia Stem Cells through In Vitro and In Vivo AML/CML Models
ROS↑, higher intracellular oxidative stress (or levels of ROS) in chronic or acute myeloid leukemia stem cells
Showing Research Papers: 1 to 9 of 9
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Ferroptosis↑, 1, GSH↓, 1, ROS↑, 6, ROS⇅, 1, ROS∅, 1, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ETC↓, 1, MMP↓, 2,
Core Metabolism/Glycolysis ⓘ
ANXA7↑, 1, CRM↑, 1,
Cell Death ⓘ
Apoptosis↑, 5, cl‑BID↑, 1, Casp8↑, 1, Casp9↑, 1, Fas↑, 1, FasL↑, 1, Ferroptosis↑, 1, JNK↑, 1, MAPK↑, 1,
Transcription & Epigenetics ⓘ
tumCV↓, 1,
Protein Folding & ER Stress ⓘ
HSP90↓, 1,
Autophagy & Lysosomes ⓘ
BNIP3↝, 1, TumAuto↑, 3,
DNA Damage & Repair ⓘ
P53↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↑, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, TumCG↓, 1, TumCG⇅, 1,
Migration ⓘ
TumCP↓, 2, TumCP⇅, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, Hif1a↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, Inflam↓, 1, NF-kB↓, 1, NF-kB↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, ChemoSen↑, 2, Dose⇅, 5, Dose↝, 1, eff↑, 1, eff∅, 1, RadioS↑, 1, selectivity↑, 1,
Functional Outcomes ⓘ
cardioP↑, 1, chemoPv⇅, 1, cognitive↑, 1, OS↑, 1, QoL↑, 1, radioP↑, 1, Risk↓, 2,
Total Targets: 53
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
GPx↑, 1, GSH↑, 1, ROS↓, 3, ROS↑, 1, ROS⇅, 1, selenoP↑, 2, SOD↓, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1,
Cell Death ⓘ
Akt↓, 1, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
other↑, 2, other↝, 2,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↑, 1, HSPs↑, 1,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 1,
Migration ⓘ
MMP9↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 1, CRP↓, 1, CXCR4↓, 1, IL17↓, 1, IL18↓, 1, IL1β↓, 1, IL6↓, 2, NF-kB↓, 1, p65↓, 1, PGE2↓, 1, TNF-α↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1, Dose⇅, 4, eff↝, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, CRP↓, 1, IL6↓, 2,
Functional Outcomes ⓘ
hepatoP↑, 1, neuroP↑, 1, toxicity↑, 1, toxicity↝, 1,
Total Targets: 44
Scientific Paper Hit Count for: Dose, Dosage
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#:% Target#:1114 State#:% Dir#:3
wNotes=on sortOrder:rid,rpid
Home Page