BioAv Cancer Research Results

BioAv, bioavailability: Click to Expand ⟱

Source:

Type: measurement

Bioavailability (usually in %) absorbed by the body.

Scientific Papers found: Click to Expand⟱

3537-

5-HTP,

5-Hydroxytryptophan: a clinically-effective serotonin precursor

Review,

NA,

*5HT↑, effective serotonin precursor
*BioAv↑, 5-HTP is well absorbed from an oral dose, with about 70 percent ending up in the bloodstream.
*BBB↑, It easily crosses the blood-brain barrier and effectively increases central nervous system (CNS) synthesis of serotonin

5309-

5-HTP,

Effects of Carbidopa on the Cerebral Accumulation of Exogenous L-5-Hydroxytryptophan in Mice

*BioAv↑, Carbidopa, an extracerebral inhibitor of L-aromatic amino acid decarboxylation, increased dose dependently the brain bioavailability of systemically administered 5-HTP

5298-

5-HTP,

Pharmacology of rising oral doses of 5-hydroxytryptophan with carbidopa

Human,

AD,

15 healthy male volunteers t

*BioAv↑, By combining 5-HTP with carbidopa (CBD), increased bioavailability for brain penetration and decreased peripheral side effects would be expected, due to reduced peripheral decarboxylation of 5-HTP to 5-HT
*Dose↝, he tolerability and subjective effects of oral 5-HTP at 100, 200 and 300 mg combined with CBD and the pharmacokinetic properties of the 5-HTP/CBD-challenge.
*toxicity↝, Frequent occurrence of nausea and vomiting limits the applicability of this challenge at 5-HTP doses above 100 mg.

5291-

5-HTP,

Kinetics of l-5-hydroxytryptophan in healthy subjects

in-vivo,

Nor,

*Half-Life↝, biological half-life of 5-HTP ranged from 2.2 to 7.4 hours, and the plasma clearnce ranged from 0.10 to 0.23 1/kg/hour.
*BioAv↑, The bioavailability of 5-HTP after oral administration in combination with carbidopa was calculated as 48% ± 15 (mean ± SD). T

5464-

AF,

Inhibition of Thioredoxin-Reductase by Auranofin as a Pro-Oxidant Anticancer Strategy for Glioblastoma: In Vitro and In Vivo Studies

vitro+vivo,

GBM,

TrxR↓, Gold derivatives are irreversible inhibitors of TrxR. Among them, auranofin (AF), a selective TrxR inhibitor, has proven its effectiveness as a drug for the treatment of rheumatoid arthritis
BioAv↓, further clinical application of AF could be challenging due to the low solubility and insufficient delivery to glioblastoma.
ROS↑, The inhibition of TrxR1, which leads to increased ROS levels, is currently recognized as the primary mechanism of AF cytotoxicity [106]. In vitro studies have also shown that AF inhibits other thioredoxin reductases, such as TrxR2 and TrxR3
eff↝, The literature indicates that not all cancer tumors exhibit the same level of TrxR expression, affecting their sensitivity to AF.
TET1?, AF was shown to inhibit TET1 in T-ALL models
BioAv↑, Encapsulating AF into nanoparticles or combining it with other pharmaceutical excipients can minimize its potential adverse effects, preserve its interaction with serum proteins, and result in greater stability.

5439-

AG,

Absorption enhancement study of astragaloside IV based on its transport mechanism in Caco-2 cells

in-vitro,

Colon,

Caco-2

BioAv↑, Both chitosan and sodium deoxycholate can increase the permeation efficiency of astragaloside IV.
BioAv↓, This study indicated that astragaloside IV having a low fraction dose absorbed in humans mainly due to its poor intestinal permeability, high molecular weight, low lipophilicity as well as its paracelluar transport may directly result in the low perm

5356-

AL,

Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects

Review,

GC,

Apoptosis↑, induction of apoptosis, inhibition of proliferation, and disruption of cancer cell signaling pathways, including the MAPK, PI3K/AKT, and NF-κB pathways.
TumCP↓,
MAPK↓,
PI3K↓,
Akt↓,
NF-kB↓,
AntiCan↑, Allicin and its other derivatives, such as diallyl disulfide (DADS) and ajoene, have been found to have strong anticancer potential both in vitro and in vivo.
ChemoSen↑, effectiveness of allicin in augmenting conventional chemotherapy and retarding tumor growth proves that allicin is one of the most efficient complementary therapies.
TumCCA↑, In liver cancer, allicin has been shown to mediate cell cycle arrest and apoptosis
Apoptosis↑,
BioAv↑, Allicin (diallyl thiosulfinate) is a compound that is generated when a garlic clove is crushed
selectivity↑, Furthermore, it has no influence on the growth of healthy intestinal cells when it causes stomach cancer cells to undergo apoptosis
TGF-β↓, Allicin can reduce the production of TGF-β2 and its receptor after directly entering gastric cancer cells.
ROS↑, It induces oxidative stress by generating reactive oxygen species (ROS), leading to DNA damage and activation of key apoptotic mediators such as phospho-p53 and p21 [81].
DNAdam↑,
p‑P53↑,
P21↑,
cycD1/CCND1↓, Additionally, cyclin D1, cyclin E, and cyclin-dependent kinases (CDKs) can all be inhibited by allicin.
cycE/CCNE↓,
CDK4↓, suppressing the CDK-4/6/cyclin D complex
CDK6↓,
MMP↓, By lowering the outer mitochondrial membrane potential (MMP), allicin raises levels of nuclear factor kappa B (NF-κB), the proapoptotic protein Bax, while decreasing the antiapoptotic protein Bcl-2, which leads to apoptosis.
NF-kB↑,
BAX↑,
Bcl-2↓,
ER Stress↑, cellular effects of allicin, including its role in inducing ER stress
Casp↑, enhancing caspase activation and apoptosis-inducing factor (AIF)-mediated cell death.
AIF↑,
Fas↑, increasing Fas receptor expression and its binding to Fas ligand (FasL), leading to apoptosis through caspase-8 and cytochrome c activation.
Casp8↑,
Cyt‑c↑,
cl‑PARP↑, leading to poly (ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation.
Ca+2↑, allicin elevates intracellular free Ca2⁺ levels, causing endoplasmic reticulum (ER) stress, which plays a critical role in apoptosis induction
*NRF2↑, by activating the Nrf2 pathway via KLF9, allicin protects against arsenic trioxide-induced liver damage,
*chemoP↑, Additionally, allicin has shown promise in reducing hepatotoxicity caused by tamoxifen (TAM), a commonly used treatment for hormone-dependent breast cancer
*GutMicro↑, Shi et al. [85] found that allicin can ameliorate high-fat diet-induced obesity in mice by altering their gut microbiome.
CycB/CCNB1↑, DATS impaired cell survival in the G2 phase by significantly upregulating cyclins A2 and B1.
H2S↑, DATS can also react with the cellular thiol glutathione to create H2S gas, which can control several other cellular functions [79].
HIF-1↓, allicin treatment (40 µg/ml) for NSCLC lowers the expression of HIF-1 and HIF-2 in hypoxic cells [73]
RadioS↑, Allicin has been shown to increase the sensitivity of X-ray radiation therapy in colorectal cancer, presumably by suppressing the levels of NF-κB, IKKβ mRNA, p-NF-κB, and p-IKKβ protein expression in vitro and in vivo

5355-

AL,

Mini-review: The health benefits and applications of allicin

Review,

Var,

*BioAv↑, another key property of allicin is its hydrophobicity, which allows it to be absorbed easily through the cell membrane without causing any physical or chemical damage to the phospholipid bilayer, thereby allowing its rapid metabolism to produce pharm
*cardioP↑, Allicin exhibits protective effects in multiple organ systems, including the brain, intestines, lungs, liver, kidneys, prostate, and heart.
*hepatoP↑,
*RenoP↑,
*Half-Life↝, half-life (t1/2)of allicin was 227 min–260 min. Because allicin is eliminated from the body by the respiratory tract, the concentration of allicin in lung tissue is significantly lower than that in the blood
*BioAv↓, We believe that the bioavailability of allicin is relatively low for the following reasons: At first, allicin is characterized by a distinctive garlic odor and chemical instability. It can be easily degraded under room temperature.
*neuroP↑, Neuroprotective activity
*cognitive↑, On the other hand, allicin improves cognitive deficits via Protein kinase R-like endoplasmic reticulum kinase (PERK)/Nuclear factor erythroid-2-related factor 2 (NRF2) signaling pathway and c-Jun N-terminal kinase (JNK) signaling pathways
*ROS↓, They found that allicin suppressed ROS generation and decreased lipid peroxidation in 6-hydroxydopamine (6-OHDA)-induced Pheochromocytoma 12 (PC12) cells
*lipid-P↓,
*DNArepair↑, Allicin not only directly protects DNA, but also indirectly protects DNA through antioxidant activity and regulation of oxidizing enzymes
*ChemoSen↑, Allicin combined with other chemotherapy drugs showed a better anti-cancer effect

3542-

ALA,

Chelation: Harnessing and Enhancing Heavy Metal Detoxification—A Review

Review,

Var,

*antiOx↑, powerful antioxidant that regenerates other antioxidants (e.g., vitamins E and C, and reduced glutathione) and has metal-chelating activity.
*VitE↑,
*VitC↑,
*GSH↑,
*IronCh↑,
*BioAv↑, Both fat and water soluble, it is readily absorbed from the gut and crosses cellular and blood-brain membrane barriers
*BBB↑,

3550-

ALA,

Mitochondrial Dysfunction and Alpha-Lipoic Acid: Beneficial or Harmful in Alzheimer's Disease?

Review,

AD,

*antiOx↑, antioxidant and anti-inflammatory properties
*Inflam↓,
*PGE2↓, α-LA has mechanisms of epigenetic regulation in genes related to the expression of various inflammatory mediators, such PGE2, COX-2, iNOS, TNF-α, IL-1β, and IL-6
*COX2↓,
*iNOS↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*BioAv↓, α-LA has rapid uptake and low bioavailability and the metabolism is primarily hepatic
*Ach↑, α-LA increases the production of acetylcholine [30], inhibits the production of free radicals [31], and promotes the downregulation of inflammatory processes
*ROS↓,
*cognitive↑, Studies have shown that patients with mild AD who were treated with α-LA showed a slower progression of cognitive impairment
*neuroP↑, α-LA is classified as an ideal neuroprotective antioxidant because of its ability to cross the blood-brain barrier and its uniform uptake profile throughout the central and peripheral nervous systems
*BBB↑,
*Half-Life↓, α-LA presented a mean time to reach the maximum plasma concentration (tmax) of 15 minutes and a mean plasma half-life (t1/2) of 14 minutes
*BioAv↑, LA consumption is recommended 30 minutes before or 2 hours after food intake
*Casp3↓, α-LA had an effect on caspases-3 and -9, reducing the activity of these apoptosis-promoting molecules to basal levels
*Casp9↓,
*ChAT↑, α-LA increased the expression of M2 muscarinic receptors in the hippocampus and M1 and M2 in the amygdala, in addition to ChaT expression in both regions.
*cognitive↑, α-LA acts on these apoptotic signalling pathways, leading to improved cognitive function and attenuation of neurodegeneration.
*eff↑, Based on their results, the authors suggest that treatment with α-LA would be a successful neuroprotective option in AD, at least as an adjuvant to standard treatment with acetylcholinesterase inhibitors.
*cAMP↑, The increase of cAMP caused by α-LA inhibits the release of proinflammatory cytokines, such as IL-2, IFN-γ, and TNF-α.
*IL2↓,
*INF-γ↓,
*TNF-α↓,
*SIRT1↑, Protein expression encoded by SIRT1 showed higher levels after α-LA treatment, especially in liver cells.
*SOD↑, antioxidant enzymes (SOD and GSH-Px) and malondialdehyde (MDA) were analysed by ELISA after 24 h of MCAO, which showed that the enzymatic activities were recovered and MDA was reduced in the α-LA-treated groups i
*GPx↑,
*MDA↓,
*NRF2↑, The ratio of nucleus/cytoplasmic Nrf2 was higher in the α-LA group 40 mg/kg, indicating that the activation of this factor also occurred in a dose-dependent manner

3546-

ALA,

Cognitive and Mood Effect of Alpha-Lipoic Acid Supplementation in a Nonclinical Elder Sample: An Open-Label Pilot Study

Study,

AD,

fifteen elder patients (mean age: 84.5 ± 5.77) received ALA at a daily dose of 600 mg/day for 12 weeks.

*antiOx↑, (ALA), a known antioxidant compound abundant in vegetables and animal tissues, in reducing oxidative stress in the aging brain and preventing cognitive decline.
*ROS↓,
*cognitive∅, no statistically significant effects either on cognitive function, executive function, or mood were found
*lipid-P↓, ALA has been shown to reduce lipid peroxidation and increase the activity of antioxidant molecules in different areas of the brain of experimental animals
*memory↑, ALA has been suggested to improve memory by increasing the activity of choline acetyltransferase (ChAT)
*ChAT↑,
*Acetyl-CoA↑, a crucial step in the biosynthesis of acetylcholine, in the hippocampi of treated rats
*Aβ↓, ALA administration can inhibit the formation of beta-amyloid fibrils and their expansion, thus exerting a direct effect on a known mechanism involved in neurodegenerative diseases
*BioAv↑, ALA is abundantly present in vegetables and animal tissues [17], is promptly bioavailable, and has no known toxic effects on animals and human subjects
*BBB↑, ALA has been demonstrated to successfully cross the blood–brain barrier in animal models
*toxicity∅, and no collateral effects have been observed at the oral daily doses currently employed as supplements (from 50 to 2400 mg/day)

297-

ALA,

Insights on the Use of α-Lipoic Acid for Therapeutic Purposes

Review,

BC,

SkBr3

Review,

neuroblastoma,

SK-N-SH

Review,

AD,

PDH↑, ALA is capable of activating pyruvate dehydrogenase in tumor cells.
TumCG↓, ALA also significantly inhibited tumor growth in mouse xenograft model using BCPAP and FTC-133 cells
ROS↑, ALA is able to generate ROS, which promote ALA-dependent cell death in lung cancer [75], breast cancer [76] and colon cancer
AMPK↑,
EGR4↓,
Half-Life↓, Data suggests that ALA has a short half-life and bioavailability (about 30%)
BioAv↝,
*GSH↑, Moreover, it is able to increase the glutathione levels inside the cells, that chelate and excrete a wide variety of toxins, especially toxic metals from the body
*IronCh↑, The existence of thiol groups in ALA is responsible for its metal chelating abilities [14,35].
*ROS↓, ALA exerts a direct impact in oxidative stress reduction
*antiOx↑, ALA is being referred as the universal antioxidant
*neuroP↑, ALA has neuroprotective effects on Aβ-mediated cytotoxicity
*Ach↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*lipid-P↓, ALA has multiple and complex effects in this way, namely scavenging ROS, transition metal ions, increasing the levels of reduced glutathione [59,63], scavenging of lipid peroxidation products
*IL1β↓, ALA downregulated the levels of the inflammatory cytokines IL-1B and IL-6 in SK-N-BE human neuroblastoma cells
*IL6↓,
TumCP↓, ALA inhibited cell proliferation, [18F]-FDG uptake and lactate formation and increased apoptosis in neuroblastoma cell lines Kelly, SK-N-SH, Neuro-2a and in the breast cancer cell line SkBr3.
FDG↓,
Apoptosis↑,
AMPK↑, ALA suppressed thyroid cancer cell proliferation and growth through activation of AMPK and subsequent down-regulation of mTOR-S6 signaling pathway in BCPAP, HTH-83, CAL-62 and FTC-133 cells lines.
mTOR↓,
EGFR↓, ALA inhibited cell proliferation through Grb2-mediated EGFR down-regulation
TumCI↓, ALA inhibited metastatic breast cancer cells migration and invasion, partly through ERK1/2 and AKT signaling
TumCMig↓,
*memory↑, Alzheimer’s Disease: ALA led to a marked improvement in learning and memory retention
*BioAv↑, Since ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
*BioAv↝, ALA were found to be considerably higher in adults with mean age greater than 75 years as compared to young adults between the ages of 18 and 45 years.
*other↓, ALA treatment has been recently studied by some clinical trials to explain its efficacy in preventing miscarriage
*other↝, 1800 mg of ALA or placebo were administrated orally every day, except during the period 2 days before to 4 days after administration of each dose of platinum to avoid potential interference with platinum’s antitumor effects
*Half-Life↓, Data shows a short half-life and bioavailability of about 30% of ALA due to mechanisms involving hepatic degradation, reduced ALA solubility as well as instability in the stomach.
*BioAv↑, ALA bioavailability is greatly reduced after food intake and it has been recommended that ALA should be admitted at least 2 h after eating or if taken before; meal should be taken at least 30 min after ALA administration
*ChAT↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*GlucoseCon↑,

4132-

Alum,

Relation between aluminum concentrations in drinking water and Alzheimer's disease: an 8-year follow-up study

Study,

AD,

*Risk↑, These findings support the hypothesis that aluminum in drinking water is a risk factor for AD. This result was confirmed for AD (adjusted relative risk=2.20, 95 percent CI 1.24–3.89)
*cognitive↓,
*BioAv↑, As suggested by Taylor,30 it is plausible that there is an increase in aluminum absorption with age, so the effect of aluminum may be larger after 75 years than before.

1557-

Api,

Preparation of apigenin nanocrystals using supercritical antisolvent process for dissolution and bioavailability enhancement

in-vitro,

Nor,

*BioAv↑, AP nanocrystals exhibited a significantly decreased tmax, a 3.6-fold higher peak plasma concentration (Cmax) and 3.4-fold higher area under the curve (AUC).

1556-

Api,

Dissolution and antioxidant potential of apigenin self nanoemulsifying drug delivery system (SNEDDS) for oral delivery

Analysis,

NA,

*BioAv↑, apigenin was developed as SNEDDS to solve its dissolution problem and enhance oral bioavailability
*Dose∅, Smix ratio of 1:1 and concentrations of Gelucire 44/14, Tween 80, and PEG 400 in the ranges of 5–40% w/w, 30–47.5% w/w, and 30–47.5% w/w, respectively, as shown in Table 1.

1554-

Api,

A Review on Flavonoid Apigenin: Dietary Intake, ADME, Antimicrobial Effects, and Interactions with Human Gut Microbiota

Review,

NA,

*BioAv↑, apigenin-7-O-glucoside, and acylated derivatives are more water soluble than apigenin [10] and their structures have a major impact on their absorption and bioavailability, with the best bioavailability occurring when apigenin is bound to β-glycoside
*BioAv↑, organic solvents like DMSO [34] and Tween 80 [31] are used to dissolve apigenin prior to their addition to an aqueous solution to increase solubility
*BioAv↑, dietary apigenin is available for metabolism by the gut microbiota
*BioAv↓, Human gut microbiota has been found to harbor enzymes that could degrade apigenin
*eff↑, This study strongly supports that the gut microbiota plays a major role in the metabolism of dietary apigenin.

1551-

Api,

Chemotherapeutic effects of Apigenin in breast cancer: Preclinical evidence and molecular mechanisms; enhanced bioavailability by nanoparticles

Review,

NA,

*BioAv↑, nanocarriers such as nanocrystals, micelles, liposomes, PLGA, etc., have highlighted the significantly increased bioavailability

1550-

Api,

Formulation and characterization of an apigenin-phospholipid phytosome (APLC) for improved solubility, in vivo bioavailability, and antioxidant potential

Analysis,

NA,

*BioAv↑, apigenin-phospholipid phytosome (APLC) was developed to improve the aqueous solubility, dissolution, in vivo bioavailability, and antioxidant activity of apigenin
*antiOx↑, exhibited antioxidant potential

1540-

Api,

Determination of Total Apigenin in Herbs by Micellar Electrokinetic Chromatography with UV Detection

Analysis,

NA,

*BioAv↑, Our assay exhibits about 40-fold lower LOD in comparison with earlier published MEKC procedure

1538-

Api,

Enhancing oral bioavailability using preparations of apigenin-loaded W/O/W emulsions: In vitro and in vivo evaluations

in-vivo,

Nor,

rats

*BioAv↑, The peak concentrations in the apigenin suspensions and the apigenin-loaded emulsions were 43.55 lg/ml and 395.47 lg/ml, respectively, indicating an approximate ninefold enhancement of oral bioavailability.

1537-

Api,

Apigenin as Tumor Suppressor in Cancers: Biotherapeutic Activity, Nanodelivery, and Mechanisms With Emphasis on Pancreatic Cancer

Review,

PC,

20-80uM

5-50mg/kg

TumCP↓,
TumCCA↑,
Apoptosis↑,
MMPs↓,
Akt↓,
*BioAv↑, delivery systems (nanosuspension, polymeric micelles, liposomes).
*BioAv↓, low solubility of apigenin in water (1.35 μg/mL) and its high permeability
Half-Life∅, (appearing in blood circulation after 3.9 h)
Hif1a↓, (HIF-1α) is targeted by apigenin in several cancers such as, ovarian cancer, prostate cancer, and lung cancer
GLUT1↓, GLUT-1 is blocked by apigenin (0–100 μM) under normoxic conditions
VEGF↓,
ChemoSen↑, apigenin can be applied as a chemosensitizer
ROS↑, accumulation of ROS produced were stimulated
Bcl-2↓, down-regulation of anti-apoptotic factors Bcl-2 and Bcl-xl as well as the up-regulation of apoptotic factors Bax and Bim.
Bcl-xL↓,
BAX↑,
BIM↑,

1558-

Api,

Preparation, characterization and antitumor activity evaluation of apigenin nanoparticles by the liquid antisolvent precipitation technique

in-vitro,

Liver,

HepG2

BioAv↑, oral bioavailability of apigenin nanoparticles was about 4.96 times higher than that of the raw apigenin
*toxicity∅, apigenin nanoparticles had no toxic effect on the organs of rats.
eff↑, higher inhibition to HepG2 cells by lower IC50 than that of raw apigenin. In addition, The IC50 values of apigenin nanoparticles and raw apigenin were separately 89.33 and 216.84 μg/mL

3822-

Aroma,

Aromatherapy in the treatment of Alzheimer's disease: A systematic review

Review,

AD,

*cognitive↑, Aromatherapy may have some potential for improving cognitive function, especially in AD patients.
*other↑, Lavandula angustifolia Mill, Salvia rosmarinus and lemon citrus:potential for improving cognitive function, especially in AD patients.
*other↓, Rosmarinus officinalis: improving cognitive function by inhaled administration
*BioAv↑, There is no doubt that components from EOs are often absorbed through the skin, enter into the circulation then cross the BBB.
*BBB?,

3391-

ART/DHA,

Antitumor Activity of Artemisinin and Its Derivatives: From a Well-Known Antimalarial Agent to a Potential Anticancer Drug

Review,

Var,

TumCP↓, inhibiting cancer proliferation, metastasis, and angiogenesis.
TumMeta↓,
angioG↓,
TumVol↓, reduces tumor volume and progression
BioAv↓, artemisinin has low solubility in water or oil, poor bioavailability, and a short half-life in vivo (~2.5 h)
Half-Life↓,
BioAv↑, semisynthetic derivatives of artemisinin such as artesunate, arteeter, artemether, and artemisone have been effectively used as antimalarials with good clinical efficacy and tolerability
eff↑, preloading of cancer cells with iron or iron-saturated holotransferrin (diferric transferrin) triggers artemisinin cytotoxicity
eff↓, Similarly, treatment with desferroxamine (DFO), an iron chelator, renders compounds inactive
ROS↑, ROS generation may contribute with the selective action of artemisinin on cancer cells.
selectivity↑, Tumor cells have enhanced vulnerability to ROS damage as they exhibit lower expression of antioxidant enzymes such as superoxide dismutase, catalase, and gluthatione peroxidase compared to that of normal cells
TumCCA↑, G2/M, decreased survivin
survivin↓,
BAX↑, Increased Bax, activation of caspase 3,8,9 Decreased Bc12, Cdc25B, cyclin B1, NF-κB
Casp3↓,
Casp8↑,
Casp9↑,
CDC25↓,
CycB/CCNB1↓,
NF-kB↓,
cycD1/CCND1↓, decreased cyclin D, E, CDK2-4, E2F1 Increased Cip 1/p21, Kip 1/p27
cycE/CCNE↓,
E2Fs↓,
P21↑,
p27↑,
ADP:ATP↑, Increased poly ADP-ribose polymerase Decreased MDM2
MDM2↓,
VEGF↓, Decreased VEGF
IL8↓, Decreased NF-κB DNA binding [74, 76] IL-8, COX2, MMP9
COX2↓,
MMP9↓,
ER Stress↓, ER stress, degradation of c-MYC
cMyc↓,
GRP78/BiP↑, Increased GRP78
DNAdam↑, DNA damage
AP-1↓, Decreased NF-κB, AP-1, Decreased activation of MMP2, MMP9, Decreased PKC α/Raf/ERK and JNK
MMP2↓,
PKCδ↓,
Raf↓,
ERK↓,
JNK↓,
PCNA↓, G2, decreased PCNA, cyclin B1, D1, E1 [82] CDK2-4, E2F1, DNA-PK, DNA-topo1, JNK VEGF
CDK2↓,
CDK4↓,
TOP2↓, Inhibition of topoisomerase II a
uPA↓, Decreased MMP2, transactivation of AP-1 [56, 88] NF-κB uPA promoter [88] MMP7
MMP7↓,
TIMP2↑, Increased TIMP2, Cdc42, E cadherin
Cdc42↑,
E-cadherin↑,

557-

ART/DHA,

Artemisinin and Its Derivatives in Cancer Care

Review,

Var,

100-250mg/d

400 mg 3x/day dosed it every other week

*BioAv↓, with High fat and high calorie meals
*BioAv↑, DHA dihydroartemisinin have improved bioavailability
Apoptosis↑,
EGFR↓,
CD31↓,
Ki-67↓,
P53↓,
TfR1/CD71↑,
P-gp↓, many artemisinin derivatives act as P-gp inhibitors
PD-1↝, Caution when used with mmunotherapy (PD1/PDL1 inhibitors)

2569-

ART/DHA,

A semiphysiological pharmacokinetic model for artemisinin in healthy subjects incorporating autoinduction of metabolism and saturable first-pass hepatic extraction

Human,

Nor,

Twenty-four healthy males

*Half-Life↝, Artemisinin was found to induce its own metabolism with a mean induction time of 1.9 h, whereas the enzyme elimination half-life was estimated to 37.9 h.
BioAv↝, Artemisinin produces a rapid onset of enzyme induction, resulting in a decrease in its own bioavailability over time.
*Half-Life↓, Plasma artemisinin concentrations reach a peak within 2–3 h after oral intake and decline with a short half-life of 1.5–2 h
BioAv↑, Artemisinin is believed to pass through the gut membrane relatively easily [3, 4], although high oral clearance values are indicative of high first-pass metabolism of the compound, resulting in low bioavailability
*Dose↝, either a daily single dose of 500 mg oral artemisinin for 5 days, or single oral doses of 100/100/250/250/500 mg on each of the first 5 days.

2577-

ART/DHA,

Artemisinin and its derivatives in cancer therapy: status of progress, mechanism of action, and future perspectives

Review,

Var,

eff↑, Artemisinin-transferrin conjugate has been shown to be more potent than artemisinin in killing cancer cells
TumCCA↑, ART has been shown to act on the G 1 phase , and DHA and ARS on the G2/M phase arrest
BioAv↑, Artemetherâ's solubility has been increased by 3- to 15-fold using pegylated lysine-based copolymeric den- dritic micelles (5-25 nm, loading 0.5-1 g/g) with prolonged release of up to 1-2 days in vitro
eff↑, ART crystals have been encapsulated with chitosan, gelatin, and alginate (766 nm) with a 90% encapsulation efficiency and improved hydrophilicity
ChemoSen↑, Combining artemisinins with chemotherapy in nano drug delivery systems can improve efficacy through higher com- bination index

5412-

ASA,

Clinical Pharmacology of Aspirin

Review,

NA,

*COX1↓, Aspirin is the acetate ester of salicylic acid and acts by binding irreversibly to cyclooxygenase-1 and cyclooxygenases-2
*COX2↓,
*cardioP↑, Aspirin is consumed most often at low-doses for cardio-protection and at higher doses as an analgesic, antipyretic, and anti-inflammatory agents.
*BioAv↑, Orally ingested aspirin is absorbed rapidly and the peak concentration is reached in about 1 hour.
*BioAv↝, a rise in pH also increases the solubility of aspirin and thus the dissolution of the tablets and the presence of food delays absorption of aspirin.
*Half-Life↓, The elimination half-life of aspirin in plasma is about 20 min
Risk↓, Patients who received 100 mg daily of aspirin had reduced risks of colorectal cancer and gastric cancer and an increased risk of gastrointestinal bleeding [6].
*other↑, Low-dose of aspirin treatment significantly improves ovarian responsiveness, uterine and ovarian blood flow velocity, and pregnancy-rates in women undergoing in-vitro fertilization [19].
*AntiAg↑, antiplatelet effect of aspirin [13],

5400-

ASA,

Beyond COX-1: the effects of aspirin on platelet biology and potential mechanisms of chemoprevention

Review,

Nor,

Risk↓, dramatically reduced incidence of cancer in individuals taking daily low-dose aspirin [1–7],
*Inflam↓, Aspirin, like the vast majority of NSAIDs, is thought to exert its anti-inflammatory effects through inhibition of cyclooxygenase enzymes (COX enzymes) that regulate the production of prostaglandins.
*COX1↓,
*AntiAg↑, spirin acts to blunt a variety of pro-inflammatory responses, including the canonical inflammatory response [9–11], production of a defensive mucosal lining [12], and platelet aggregation [13, 14].
*Half-Life↓, The half-life of aspirin in the bloodstream was previously shown to be 13–19 min with a non-enzymatic hydrolysis rate of 0.023 min−1 at 37 °C in individuals given a single oral administration of aspirin.
*BioAv↑, Approximately 70% of aspirin reaches the peripheral circulation intact with maximum serum concentrations observed at 25 min after administration.

3154-

Ash,

Pharmacokinetics and bioequivalence of Withania somnifera (Ashwagandha) extracts – A double blind, crossover study in healthy adults

BioAv↑, The longer half-life and higher mean residence time of the higher strength extract WS-35, which contained 35% withanolide glycosides, demonstrated its enhanced oral bioavailability
BioAv↓, Singh et al. [20] tested the bioavailability of withaferin A (purity 99%) by oral (25 mg/kg) and withanoside IV (2 mg/kg) routes in Sprague Dawley rats and found its oral bioavailability to be poor (approximately 5%) despite rapid distribution after

5385-

AsP,

GoldNP,

GEM,

Development of ascorbyl palmitate based hydrophobic gold nanoparticles as a nanocarrier system for gemcitabine delivery

in-vitro,

BC,

 0.44 μg/mL

 The Au-GEM-
AsP-MOD

ROS↑, At pharmacologic concentrations, ascorbate undergoes oxidation via ascorbate radical, generating cytotoxic hydrogen peroxide (H₂O₂) through Fenton chemistry
Fenton↑,
BioAv↑, Although AsP is more stable than vitamin C, its poor release capacity and water insolubility limit its bioavailability and therapeutic efficacy15,17. Thus, incorporating it into nanoparticle carriers can enhance circulation time and tumor accumulatio
EPR↑, Nanoparticles sized 30–200 nm enhance cell uptake via increased surface area and membrane wrapping, effectively accumulating in tumors

5387-

AsP,

PacT,

Ascorbyl palmitate-incorporated paclitaxel-loaded composite nanoparticles for synergistic anti-tumoral therapy

in-vivo,

Melanoma,

B16-F10

Dose↝, we developed a dual drug delivery system to encapsulate ascorbyl palmitate (AP) and paclitaxel (PTX) for synergistic cancer therapy. 223 nm
TumCG↓, In vivo, AP/PTX-SLNs were revealed to be much more effective in suppressing tumor growth in B16F10-bearing mice and in eliminating cancer cells in the lungs
TumCP↓, AP has been found to inhibit the cell proliferation and DNA synthesis of various cancer cells, including breast, colon, glioblastoma, skin, and brain cancer cells (Naidu, 2003a).
BioAv↓, AP is limited due to its water insolubility, rapid degradation (accelerated by metal ions and/or light), and low bioavailability.
BioAv↑, Therefore, new technologies including nanoparticles that can enhance its delivery efficacy and reduce the dose of administration for Vc while not reducing its anti-cancer efficacy are highly desired.
other↑, These results conformed to the conclusion that only high doses of ascorbic acid have the ability to induce cancer cell death.
Apoptosis↑, Conclusively, the AP/PTX-SLNs exhibited a greater efficacy in inducing cell apoptosis by reducing the Bcl-2/Bax ratio accompanied by promoting tubulin polymerization
Bax:Bcl2↑,
EPR↑, such nanocarriers to permeate into tumor sites because of the enhanced permeation and retention (EPR) effect.
toxicity↝, AP/PTX synergistic combination-based SLN therapy did not induce toxicity and represents a promising strategy for paclitaxel/the vitamin C derivative in promoting anti-cancer effects.

1146-

AsP,

Potential use of nanoformulated ascorbyl palmitate as a promising anticancer agent: First comparative assessment between nano and free forms

in-vivo,

Nor,

Ehrlich ascites carcinoma (EAC)-bearing mice

TumCCA↑, G2/M phase
Apoptosis↑,
IL6↓,
STAT3↓,
angioG↓,
TumMeta↓,
VEGF↓,
MMP9↓,
SOD↑,
Catalase↑,
GSH↓,
MDA↓,
NO↓,
*BioAv↑, nano particles

4804-

ASTX,

Astaxanthin in cancer therapy and prevention (Review)

Review,

Var,

Review,

AD,

*antiOx↑, gained significant attention for its potent antioxidant, anti-inflammatory and anti-proliferative properties.
*Inflam↓,
ChemoSen⇅, In some instances, it reduces the cytotoxicity of cisplatin, particularly with cisplatin on the SKBR3 breast cancer cell line, indicating a potential protective effect. In certain cases, AXT enhances the cytotoxic effect of the chemotherapy drugs
chemoP↑, The present review detailed both in vitro and in vivo studies highlighting the effectiveness of AXT in sensitizing cancer cells to chemotherapy, thereby enhancing therapeutic outcomes and potentially reducing treatment-related side effects.
BioAv↑, incorporation of AXT in nanoparticle-based delivery systems has further improved its bioavailability
TumCP↑, AXT exhibits hormetic effects on U251-MG, T98G and CRT-MG cell lines, where low doses stimulate cell proliferation
ROS⇅, while higher doses induce apoptosis by triggering a dose-dependent oxidative stress response, significantly increasing reactive oxygen species (ROS) levels and promoting apoptosis
Apoptosis↑,
PI3K↑, AXT activates the PI3K/Akt/GSK3β pathway, leading to the upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor, in SH-SY5Y cells under oxygen and glucose deprivation conditions
Akt↑,
GSK‐3β↑,
NRF2↑,
AntiCan↑, antioxidant, AXT has the potential to act as both an anticancer drug and a neuroprotectant.
*neuroP↑, AXT protects against oxidative stress, which causes mitochondrial dysfunction and apoptosis, thereby reducing the detrimental effects associated with neurodegenerative diseases such as Alzheimer's, Parkinson's
eff↑, The synergistic cytotoxic effect of AXT with melatonin showed enhanced efficacy in the T47D cell line compared with the MDA-MB-231 line
AntiTum↑, AXT effectively reduced tumor size and the number of cancer cells in mice, supporting its potential anti-tumor activity.

4807-

ASTX,

An overview of the anticancer activity of astaxanthin and the associated cellular and molecular mechanisms

Review,

Var,

*antiOx↑, Reports indicate that ASX’s antioxidant efficacy surpasses that of vitamin C, vitamin E, coenzyme Q10, and alpha-lipoic acid.
*neuroP↑, Astaxanthin is a powerful antioxidant compound that supports heart, skin, and eye health, helps manage diabetes, and offers brain-protective benefits.
AntiCan↑, Astaxanthin shows promise as an anticancer agent by limiting tumor growth, inducing cancer cell death, and reducing the spread of malignant cells.
TumCG↓,
TumCD↑,
TumCMig↓,
ChemoSen↑, Astaxanthin enhances the effects of chemotherapy, reduces its side effects, and helps overcome drug resistance.
chemoP↑,
*BioAv↓, Astaxanthin has limited absorption in the body, but using nanocarriers like nanoparticles and nano-emulsions can greatly enhance its bioavailability and therapeutic potential.
TumCP↓, ASX inhibits tumor formation, primarily by hindering cell proliferation, inducing cell cycle arrest, and promoting apoptosis.
TumCCA↑,
Apoptosis↑,
BioAv↑, Nanotechnology: a solution for improving astaxanthin bioavailability

5427-

ASTX,

Astaxanthin and Cancer Chemoprevention

Review,

Var,

chemoP↑, evidence for anticarcinogenic behavior of selected carotenoids, with an emphasis on the chemopreventive activities of astaxanthin.
AntiCan↑, Human epidemiological studies have revealed a protective effect of vegetable and fruit consumption for cancers of the stomach, esophagus, lung, oral cavity and pharynx, bladder, endometrium, pancreas, colon and rectum, breast, cervix, ovary and prost
chemoPv↑, the chemopreventive effects of canthaxanthin
Risk↓, Salmon, the principal dietary source of astaxanthin, is an important component of the traditional diets of Eskimos and certain coastal tribes in North America; these groups have shown unusually low prevalence of cancer.
lipid-P↓, Dietary astaxanthin also reduced metastatic nodules and lipid peroxidation in the livers of rats treated with restraint stress.
Pain↓, The results revealed that astaxanthin significantly relieved pain and improved performance in patients with RA
BioAv↑, the results demonstrated an enhancement of astaxanthin bioavailability in humans when incorporated into lipid-based formulations.
Dose↝, relevant dietary dosages of astaxanthin (4-12 mg daily is typically recommended by supplement manufacturers),

5417-

ASTX,

Comparative Pharmacokinetic Study of Standard Astaxanthin and its Micellar Formulation in Healthy Male Volunteers

Study,

Nor,

*antiOx↑, Astaxanthin is a naturally occurring carotenoid with high anti-oxidant properties
*BioAv↓, but it is a very lipophilic compound with low oral bioavailability. The oral bioavailability of astaxanthin ranges around 10–50% of the given dose, as a result of its poor solubility in water and poor absorption by epithelial cells of the small intes
*Dose↝, compare the pharmacokinetic parameters of a novel astaxanthin preparation based on micellar solubilization technology, NovaSOL® 400-mg capsules (Test product), and those of astaxanthin 400-mg capsules (reference product),
*BioAv↑, The test micellar astaxanthin reached a Cmax of 7.21 µg/ml after 3.67 h compared to only 3.86 µg/ml after 8.5 h for the reference native astaxanthin.

5419-

ASTX,

Astaxanthin and other Nutrients from Haematococcus pluvialis—Multifunctional Applications

Review,

Nor,

*antiOx↑, extraction of astaxanthin and analysis of its antioxidant, anti-inflammatory, anti–diabetic and anticancer activities.
*Inflam↓,
*AntiDiabetic↓,
AntiCan↑,
*lipid-P↓, astaxanthin is more effective than β-carotene in the prevention of lipid peroxidation.
TumCP↓, Studies have reported that astaxanthin not only inhibits the proliferation of colon cancer cells but can also cause their apoptosis
Apoptosis↑,
TumCCA↑, Astaxanthin was included in the extract and was responsible for stopping the progression of the cell cycle and promoting the apoptosis [95].
*SOD↑, Astaxanthin also increased SOD activity and decreased PG-E2, LT-B4, NO, IL-8 and IFN- γ production [103,104,105].
*PGE2↓,
*NO↓,
*IL8↓,
*IFN-γ↓,
*cardioP↑, Astaxanthin has a cardiovascular protective effect in animals, but there is a lack of research supporting the therapeutic benefit of astaxanthin in atherosclerotic cardiovascular disease in humans.
*NF-kB↓, Oral supplementation with astaxanthin in rats after surgery decreased the expression of NF-KB and TNF-α,
*TNF-α↓,
*BioAv↑, Satisfactory astaxanthin bioavailability results were obtained with a daily astaxanthin dose of 40 mg/day.

5420-

ASTX,

A New Tailored Nanodroplet Carrier of Astaxanthin Can Improve Its Pharmacokinetic Profile and Antioxidant and Anti-Inflammatory Efficacies

in-vivo,

Nor,

*eff↑, Astaxanthin (ATX) is a carotenoid nutraceutical with poor bioavailability due to its high lipophilicity. We tested a new tailored nanodroplet capable of solubilizing ATX in an oil-in-water micro-environment (LDS-ATX) for its capacity to improve the A
*SOD↑, SOD activity was restored only by LDS-ATX in the liver and brain and by both ATX and LDS-ATX in muscle.
*BioAv↑, These results strongly suggest an organ-dependent improvement of ATX bioavailability and efficacy by the LDS-ATX nanoformulation.

5422-

ASTX,

Improved intestinal absorption and oral bioavailability of astaxanthin using poly (ethylene glycol)-graft-chitosan nanoparticles: preparation, in vitro evaluation, and pharmacokinetics in rats

in-vivo,

Nor,

*antiOx↑, Astaxanthin (ASTA) is a kind of food-derived active ingredient (FDAI) with antioxidant and antidiabetic functions.
*AntiDiabetic↑,
*toxicity∅, It is nontoxic but its poor solubility and low bioavailability hinder its application in the food industry.
*BioAv↓,
*BioAv↑, n this study, a novel carrier, polyethylene glycol-grafted chitosan (PEG-g-CS) was applied to enhance the bioavailability of astaxanthin.

5423-

ASTX,

Pharmacokinetic Profile of Astaxanthin Nanoemulsion Using HPLC (High-Performance Liquid Chromatography) With Oral Routes

in-vivo,

Nor,

*BioAv↓, Astaxanthin is a very strong antioxidant of the xanthophyll carotenoid group with very lipophilic properties, so in oral administration, its bioavailability is very low
*antiOx↑,
*BioAv↑, The results showed that in the astaxanthin nanoemulsion, there was an increasing in Cmax and AUC0-∞ which affected increasing the bioavailability value.
*Half-Life↝, This is shown in pure astaxanthin, and the t1/2 elimination calculation is 22.53 hours longer than the astaxanthin nanoemulsion, which is a 14.50-hour t1/2 elimination.

5364-

AV,

A New Biomaterial Derived from Aloe vera—Acemannan from Basic Studies to Clinical Application

Review,

Var,

BioAv↑, Acemannan (AC) is considered to be a natural polysaccharide with good biodegradability and biocompatibility extracted from Aloe vera
AntiTum↑, AC has the potential to treat various diseases, such as oral diseases, systemic metabolic diseases, cardiovascular system diseases, and benign and malignant tumors [12].
cardioP↑,

5568-

B-Gluc,

immuno,

Beta-glucans in oncology: revolutionizing treatment with immune power & tumor targeting

Review,

Var,

TNF-α↓, Beta-glucans suppress pro-inflammatory cytokines (e.g., TNF-α, IL-6) and tumor-promoting pathways like NF-κB, while modulating T-regulatory cells (Tregs) and downregulating PD-L1 to overcome immune evasion.
IL6↓,
NF-kB↓,
PD-L1↓,
Imm↑,
BAX↑, They induce apoptosis via Bax/Bcl-2 regulation, arrest cell cycles at G1/S or G2/M phases, and inhibit angiogenesis by targeting VEGF and MMPs.
Bcl-2↓,
TumCCA↑,
angioG↓,
VEGF↓,
MMPs↓,
OS↑, improved overall survival (OS) in melanoma (hazard ratio
chemoP↑, alongside reduced chemotherapy toxicity
eff↑, Synergy with PD-1/PD-L1 inhibitors enhances immunotherapy efficacy, particularly in immunogenic tumors.
BioAv↑, Advanced nano-delivery systems, including micelles and exosomes, improve bioavailability and tumor targeting.

5574-

B-Gluc,

Beta Glucan: Health Benefits in Obesity and Metabolic Syndrome

Review,

Obesity,

*BioAv↑, β-glucan is a relatively inexpensive milling byproduct, and it is added to foods on the assumption that this will contribute to health benefits.
*toxicity↓, Moreover, no human adverse effects have been reported following the consumption of a diet rich in β-glucan from oat or barley flour or their extracts [70].
*Imm↑, Among polysaccharides that act as immunostimulants, β-glucans were found to be the most effective against infectious diseases and cancer [88].
*eff↑, The immunological potency of β-glucans varies with the molecular mass, solution conformation, backbone structure, degree of branching as well as the cell type that is targeted [89].
*Risk↓, pretreatment of high-risk surgical patients with intravenous yeast β-(1,3; 1,6)-D-glucan decreased the infection incidence, shortened intensive care unit length stay, and improved survival in comparison to a saline placebo injection
*Weight↓, In this particular study, chitin-glucan decreased high fat diet-induced body weight gain, fat mass development, fasting hyperglycemia, glucose intolerance,
*eff↝, A drink containing 5 g of oat β-glucan with a molecular weight 70 000 Da significantly lowered postprandial glucose and insulin levels relative to a rice drink control, while a similar drink containing barley β-glucan 40 000 Da had no effect
*BP↓, 8 g/day of supplemented soluble fiber from oat bran over 12 weeks significantly reduced both systolic and diastolic blood pressure in comparison to the control [197].
*GutMicro↑, Beta glucans selectively support the growth of Lactobacilli and Bifidobacteria, both of them being antagonists to pathogenic bacteria in the digestive system [
*eff↓, freeze-thaw cycle reduced the solubility of β-glucan in oat bran muffins by 9% to 55% of the fresh values.

5508-

Ba,

Neuroprotective effects of baicalin and baicalein on the central nervous system and the underlying mechanisms

Review,

Stroke,

Review,

Park,

Review,

AD,

*neuroP↑, Recent studies have shown its good protective effect on neurons and brain tissues [14].
*antiOx↑, strong anti-inflammatory and antioxidant properties.
*Inflam↓,
*BioAv↝, When taken orally, baicalin is converted to baicalein via β-glucuronidase (GUS), which is produced by the intestinal flora.
*BioAv↑, Pharmacokinetics indicate that baicalein has a higher absorption rate than baicalein [19], but once it is absorbed, baicalein is quickly degraded in the bloodstream, yielding baicalein
*Half-Life↝, The distribution half-life and elimination half-life of baicalin in the CSF of normal rats are 0.8868 and 26.0968 min, respectively.
*TLR4↓, Inhibition of the TLR4/MyD88/NF-κB signal
*NF-kB↓,
*iNOS↓, decreasing the synthesis of iNOS, COX2, and TNF-α
*COX2↓,
*TNF-α↓,
*12LOX↓, downregulation of 12/15-LOX after cerebral ischemia
*NLRP3↓, Inhibition of the expression of NLRP3, HT-22 cells
*ROS↓, Decrease in the ROS levels in the ICH, thus inhibiting high NLRP3
*IL1β↓, Reduced the amounts of IL-1β and IL-6 and inhibited the activation of the NLRP3 inflammasome
*IL6↓,
*GSK‐3β↓, Inhibiting the activation of the GSK3β/NF-κB/NLRP3 signaling pathway
*NRF2↑, Fang et al. reported that the activation of the Akt pathway resulted in increased Nrf2 nuclear translocation and immunoreactivity in a group treated with baicalin
*BBB↑, baicalein effectively crosses the blood‒brain barrier (BBB) and stimulates the Nrf2/HO-1 pathway via specialized brain-targeted exosomes
*SOD↑, increased serum levels of SOD and GSH-Px.
*GPx↑,
*MDA↓, baicalin inhibited the ROS production and reduced MDA levels in brain tissues from a rat model of cerebral I/R injury induced by middle cerebral artery occlusion (MCAO).

5506-

Ba,

Improved Bioavailability and Hepatoprotective Activity of Baicalein Via a Self-assembled Solutol HS15 Micelles System

in-vivo,

Nor,

carbon tetrachloride (CCl4) induced acute liver injury.

*AST↓, The in vivo results showed that HS15-BA micelles significantly inhibited the activity of the CCl4-induced liver injury marker enzymes aspartate transaminase (AST) and alanine transaminase (ALT).
*ALAT↓,
*GSH↓, leading to increased L-glutathione (GSH) and superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) activity, while HS15-BA significantly reversed the above changes.
*SOD↓,
*MDA↓,
*hepatoP↑, BA also had a hepatoprotective effect through anti-inflammatory activity;
*Inflam↓,
BioAv↑, In summary, our study confirmed that HS15-BA micelles enhanced the bioavailability of BA, and showed hepatoprotective effects through antioxidant and anti-inflammatory activities.

5503-

Ba,

Preparation, pharmacokinetics and biodistribution of baicalin-loaded liposomes

Study,

Nor,

*BioAv↑, The oral bioavailability and the peak concentration of the BA-LP was threefold and 2.82-fold that of BA-CMC, respectively.

5500-

Ba,

Safety, tolerability, and pharmacokinetics of oral baicalein tablets in healthy Chinese subjects: A single‐center, randomized, double‐blind, placebo‐controlled multiple‐ascending‐dose study

Trial,

Nor,

healthy subjects were randomized to receive 200, 400, and 600 mg of baicalein tablet or placebo once daily on day 1 and day 10, 3 times daily on days 4–9.

Thirty‐six healthy subjects

*toxicity↓, Baicalein tablet was generally safe and well‐tolerated.
*BioAv↑, Oral baicalein tablets were rapidly absorbed with peak plasma levels being reached within 2 h after multiple administration.
*Half-Life↝, highest urinary excretion of baicalein and its metabolites peaked in 2 h, followed by 12 h, with a double peak trend.
*Dose↝, steady‐state concentration of baicalein was achieved after 6 days of multiple dosing, and the mean Cavg and AUC0–τ,ss of baicalein were 633.64 (290.36) ng/ml and 5069.16 (2322.87) h ng/ml for 600 mg.

5496-

Ba,

A strategy to improve the oral availability of baicalein: The baicalein-theophylline cocrystal

in-vivo,

Nor,

*BioAv↓, Due to its poor water solubility (16.82 μg/ml), the therapeutic effectiveness and oral bioavailability of Baicalein are highly limited.
*BioAv↑, BE-TH cocrystals demonstrated 2.2-fold and 7.1-fold higher rate of dissolution than that of BE coarse powder in HCl (pH = 1.2) and phosphate buffer (PBS, pH = 6.8), respectively.

5250-

Ba,

Exploring baicalein: A natural flavonoid for enhancing cancer prevention and treatment

Review,

Var,

Apoptosis↑, Baicalein is thought to prevent cancer progression by inducing apoptosis, autophagy, and genome instability, and its ability to promote chemo-potentiation, anti-metastatic effects, and regulate specific signalling molecules and transcription factors.
TumAuto↑,
DNAdam↑,
*antiOx↑, Baicalein has already been proven to be a radical scavenger that acts as an antioxidant [14,15
Inflam↓, it can also reduce inflammation [16] and act as an E2 prostaglandin inhibitor [17].
PGE2↓,
TumCCA↑, Baicalein properties prevent cell proliferation, induce apoptosis, autophagy, cell cycle arrest, cancer cell migration and invasion, and decrease angiogenesis [18,19].
TumCMig↓,
TumCI↓,
angioG↓,
selectivity↑, Furthermore, some studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells.
ChemoSen↑, the current review emphasises baicaleins' synergistic potential with other chemotherapeutic agents
HIF-1↓, baicalein against ovarian cancer by demonstrating that it can limit tumour cell viability by downregulating the expression of cancer-promoting genes such as HIF-1, cMyc, NFkB, and VEGF
cMyc↓,
NF-kB↓,
VEGF↓,
P53↑, Baicalein has been shown to activate p53, a tumour suppressor protein that regulates cell growth and division [26].
MMP2↓, anticancer properties of baicalein are mediated through various molecular mechanisms, including inhibition of MMP-2;
CSCs↓, inhibition of cancer stem cells
Bcl-xL↓, after bladder cancer cells were treated with baicalein, the expression of antiapoptotic genes (Bcl2, Bcl-xL, XIAP, and survivin) was reduced, and cell viability was decreased [38].
XIAP↓,
survivin↓,
tumCV↓,
Casp3↑, upregulating the expression of caspase-3 and caspase-8 and decreased the BCL-2/BAX ratio [16]
Casp8↑,
Bax:Bcl2↑,
Akt↓, in lung cancer cells, apoptosis was induced through the downregulation of the Akt/mTOR signalling pathway [25].
mTOR↓,
PCNA↓, baicalein treatment promoted apoptosis in mice with U87 gliomas by downregulating PCNA expression, enhancing the expression of caspase-3 and caspase-9 and improving the Bax/Bcl-2 ratio
MMP↓, baicalein treatment of lung cancer cells caused a collapse of the mitochondrial membrane potential (MMP), an increase in ROS generation, and enhanced PARP, caspase 3, and caspase 9 cleavage,
ROS↑,
PARP↑,
Casp9↑,
BioAv↑, Baicalein has been found to enhance the cytotoxicity and bioavailability of certain cancer therapy drugs when combined [85]
eff↑, combination of baicalein with silymarin differentially decreased the viability of HepG2 cells, enhanced the proportion of cells in the G0/G1 phase, upregulated tumour suppressors such as Rb and p53 and CDK inhibitors, and downregulated cyclin D1, cyc
P-gp↓, By inhibiting P-glycoprotein (P-gp), baicalein can increase the accumulation of chemotherapeutic drugs within cancer cells [21]
BioAv↑, selenium–baicalein nanoparticles as a targeted therapeutic strategy for NSCLC. This strategy significantly improves the bioavailability of baicalein through several mechanisms.
selectivity↑, ome studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells

Showing Research Papers: 1 to 50 of 328
Page 1 of 7 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 328

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 13, GPx↑, 2, GSH↓, 1, GSH↑, 2, lipid-P↓, 4, MDA↓, 3, NRF2↑, 3, ROS↓, 5, SOD↓, 1, SOD↑, 4, VitC↑, 1, VitE↑, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 2,

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1, Acetyl-CoA↑, 1, ALAT↓, 1, cAMP↑, 1, GlucoseCon↑, 1, SIRT1↑, 1,

Cell Death ⓘ

Casp3↓, 1, Casp9↓, 1, iNOS↓, 2,

Transcription & Epigenetics ⓘ

Ach↑, 2, other↓, 2, other↑, 2, other↝, 1,

DNA Damage & Repair ⓘ

DNArepair↑, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1,

Migration ⓘ

AntiAg↑, 2,

Angiogenesis & Vasculature ⓘ

NO↓, 1,

Barriers & Transport ⓘ

BBB?, 1, BBB↑, 5,

Immune & Inflammatory Signaling ⓘ

COX1↓, 2, COX2↓, 3, IFN-γ↓, 1, IL1β↓, 3, IL2↓, 1, IL6↓, 3, IL8↓, 1, Imm↑, 1, INF-γ↓, 1, Inflam↓, 6, NF-kB↓, 2, PGE2↓, 2, TLR4↓, 1, TNF-α↓, 4,

Synaptic & Neurotransmission ⓘ

5HT↑, 1, ChAT↑, 3,

Protein Aggregation ⓘ

Aβ↓, 1, NLRP3↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 10, BioAv↑, 36, BioAv↝, 3, ChemoSen↑, 1, Dose↝, 4, Dose∅, 1, eff↓, 1, eff↑, 4, eff↝, 1, Half-Life↓, 5, Half-Life↝, 6,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1, BP↓, 1, GutMicro↑, 2, IL6↓, 3,

Functional Outcomes ⓘ

AntiDiabetic↓, 1, AntiDiabetic↑, 1, cardioP↑, 3, chemoP↑, 1, cognitive↓, 1, cognitive↑, 4, cognitive∅, 1, hepatoP↑, 2, memory↑, 2, neuroP↑, 6, RenoP↑, 1, Risk↓, 1, Risk↑, 1, toxicity↓, 2, toxicity↝, 1, toxicity∅, 3, Weight↓, 1,
Total Targets: 83

Scientific Paper Hit Count for: BioAv, bioavailability

19 chitosan
16 Curcumin
16 Selenium NanoParticles
13 Pterostilbene
13 Sulforaphane (mainly Broccoli)
10 Apigenin (mainly Parsley)
9 Quercetin
9 Chlorogenic acid
9 EGCG (Epigallocatechin Gallate)
8 Astaxanthin
8 borneol
8 Lycopene
8 Resveratrol
8 Thymoquinone
7 Baicalein
7 Berberine
7 Capsaicin
7 Carvacrol
7 Piperlongumine
7 Rosmarinic acid
7 Urolithin
5 Betulinic acid
5 Chrysin
5 Piperine
5 Phenethyl isothiocyanate
4 5-Hydroxytryptophan
4 Alpha-Lipoic-Acid
4 Artemisinin
4 Boswellia (frankincense)
4 Thymol-Thymus vulgaris
4 Honokiol
4 Luteolin
4 Phenylbutyrate
4 Silymarin (Milk Thistle) silibinin
3 Ascorbyl Palmitate
3 Gold NanoParticles
3 Biochanin A
3 Boron
3 Lecithin
3 Naringin
3 Selenite (Sodium)
3 Vitamin C (Ascorbic Acid)
2 Allicin (mainly Garlic)
2 Aspirin -acetylsalicylic acid
2 Paclitaxel
2 beta-glucans
2 immunotherapy
2 Berbamine
2 Celastrol
2 Folic Acid, Vit B9
2 Chlorophyllin
2 Chocolate
2 Propolis -bee glue
2 Coenzyme Q10
2 Camptothecin
2 Copper and Cu NanoParticles
2 Disulfiram
2 Ellagic acid
2 Fisetin
2 Shilajit/Fulvic Acid
2 Gallic acid
2 Magnetic Fields
2 nicotinamide adenine dinucleotide
2 Niclosamide (Niclocide)
2 Selenium
2 Spermidine
2 Aflavin-3,3′-digallate
1 Auranofin
1 Astragalus
1 Aluminum
1 Aromatherapy
1 Ashwagandha(Withaferin A)
1 Gemcitabine (Gemzar)
1 Aloe anthraquinones
1 Docetaxel
1 Radiotherapy/Radiation
1 beta-carotene(VitA)
1 Bicalutamide
1 Caffeic acid
1 Melatonin
1 Carnosic acid
1 urea
1 capecitabine
1 Catechins
1 Cannabidiol
1 Choline
1 irinotecan
1 Crocetin
1 Silver-NanoParticles
1 Citric Acid
1 Electrical Pulses
1 Ferulic acid
1 Fenbendazole
1 flavonoids
1 Kaempferol
1 MCToil
1 Gambogic Acid
1 Genistein (soy isoflavone)
1 HydroxyCitric Acid
1 itraconazole
1 Metformin
1 Magnesium
1 magnetic nanoparticles
1 Bicarbonate(Sodium)
1 Oleuropein
1 Oxygen, Hyperbaric
1 Psoralidin
1 Parthenolide
1 Rutin
1 Chemotherapy
1 Date Fruit Extract
1 Shikonin
1 Vitamin B3,Niacin
1 Vitamin E
1 Vitamin K2

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#:792  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

BioAv Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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