AntiP Cancer Research Results

AntiP, antiparasitic: Click to Expand ⟱

Source:

Type:

Antiparasitic Activity - Activity Against Parasitic Organisms

Type: Therapeutic effect / antimicrobial functional outcome

Function: Antiparasitic activity refers to the ability of a compound, extract, drug, or intervention to inhibit the growth, survival, replication, development, or infectivity of parasitic organisms. Depending on the study, this may include protozoa, helminths, or ectoparasites.

Favorable Direction: ↑ Antiparasitic activity = greater inhibition or killing of parasites and is generally favorable.

Unfavorable Direction: ↓ Antiparasitic activity = reduced effectiveness against parasites.

Scientific Papers found: Click to Expand⟱

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

8038-

IVM,

Ivermectin and gemcitabine combination treatment induces apoptosis of pancreatic cancer cells via mitochondrial dysfunction

in-vitro,

PC,

*AntiP↑, Ivermectin, an antiparasitic drug, exerts antitumor effects in various cancer types.
AntiTum↑,
ChemoSen↑, ivermectin–gemcitabine combination treatment suppressed pancreatic cancer more effectively than gemcitabine alone treatment.
TumCP↓, ivermectin–gemcitabine combination inhibited cell proliferation via G1 arrest of the cell cycle, as evidenced by the downregulation of cyclin D1 expression and the mammalian target of rapamycin (mTOR)/signal transducer and activator of transcriptio
TumCCA↑,
cycD1/CCND1↓,
mTOR↓,
STAT3↑, and activator of transcription 3 (STAT-3) signaling pathway.
Apoptosis↑, Ivermectin–gemcitabine increased cell apoptosis by inducing mitochondrial dysfunction via the overproduction of reactive oxygen species and decreased the mitochondrial membrane potential.
mtDam↑,
ROS↑,
MMP↓,
OCR↓, combination treatment also decreased the oxygen consumption rate and inhibited mitophagy, which is important for cancer cell death.
MitoP↓,

8036-

IVM,

Ivermectin inhibits the growth of ESCC by activating the ATF4-mediated endoplasmic reticulum stress-autophagy pathway

in-vitro,

ESCC,

KYSE-30

*AntiP↑, Ivermectin is a broad-spectrum antiparasitic drug with notable antitumor activity.
AntiTum↑,
ER Stress↑, we elucidate the role of ivermectin in ESCC suppression by activating the endoplasmic reticulum (ER) stress and autophagy pathways.
TumAuto↑,
ATF4↑, activating transcription factor 4 (ATF4) and DNA damage inducible transcript 3 (DDIT3) are involved in the activation of ER stress by ivermectin. show that ivermectin activates the expression of ATF4, a regulator of the ER stress pathway.
CHOP/DDIT3↝,
TumCG↓, ivermectin treatment suppresses the growth of ESCC xenograft tumors in nude mice.
PERK↑, Furthermore, the increase in the protein levels of PERK, CHOP, and ATF4 suggested that ER stress was induced.
ROS↑, Ivermectin induces ATF4 and autophagy through ROS generation
*toxicity↓, Ivermectin has been used in millions of parasite-infected patients and is well tolerated; therefore, it has been proven to be safe at its antiparasitic dosage
Ca+2↑, We demonstrated here that ivermectin activated ER stress and increased ROS and Ca 2+ levels in ESCC cells.

8035-

IVM,

Ivermectin and non-parasitic disorders: An update

Review,

Var,

Review,

AD,

Review,

Stroke,

*AntiP↑, Ivermectin, a broad-spectrum anti-parasitic agent, demonstrates potential therapeutic benefits in treating non-parasitic ailments, particularly in neurological, respiratory, inflammatory, dermal, cardiovascular, and neoplastic disorders.
angioG↓, inhibits angiogenesis, and has anti-cancer properties,
*AntiCan↓,
mtDam↑, inducing mitochondrial dysfunction, apoptosis, necrosis, and autophagy, as well as promoting oxidative stress.
Apoptosis↑,
necrosis↑,
TumAuto↑,
ROS↑,
*neuroP↑, Recent discoveries have revealed the neuroprotective effects of ivermectin in cerebral ischemia/reperfusion and Alzheimer's disease.
*Stroke↝, However, a recent study suggested that ivermectin pre-treatment may have detrimental effects on myocardial ischemia.
*cardioP↑, some studies have reported cardioprotective effects of ivermectin.

8031-

IVM,

Antiparasitic agents in oncology: Innovative mechanisms, emerging evidence and clinical potential in cancer treatment

*AntiP↑, Drugs originally developed to treat parasitic infections, including ivermectin, mebendazole, niclosamide, albendazole, artesunate, flubendazole, and other antiparasitic agents, have demonstrated compelling anticancer properties across a wide range of
Wnt↓, inhibition of key oncogenic pathways (including Wnt/β-catenin, PI3K/Akt/mTOR, and Hedgehog signaling), immunomodulation, and targeting cancer stem cell populations.
β-catenin/ZEB1↓,
PI3K↓,
Akt↓,
mTOR↓,
HH↓,
Imm↑, immunostimulatory properties
CSCs↓,
P-gp/ABCB1↓, modulation of the P-glycoprotein drug efflux pump, activation of chloride ion channels, and inhibition of oncogenic signaling.
Chl↓,
angioG↓, demonstrated anti-angiogenic

8029-

IVM,

Ivermectin in Cancer Treatment: Should Healthcare Providers Caution or Explore Its Therapeutic Potential?

Review,

Var,

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.

8027-

IVM,

Progress in Understanding the Molecular Mechanisms Underlying the Antitumour Effects of Ivermectin

Review,

Var,

*AntiP↑, Ivermectin was soon adopted in 1987 as a human medicine that was originally used for the treatment of onchocerciasis, a parasitic infection.
TumCD↑, Ivermectin causes cell death in cancer cell lines by inducing PAK1-mediated cytostatic autophagy,
PAK1↑,
TumAuto↑,
Casp↑, caspase-dependent apoptosis and immunogenic cell death (ICD) through the modulation of some pathways, including the WNT-T cell factor (TCF), Hippo and Akt/mTOR pathways.
ICD↑,
TCF↝, Ivermectin Serves as a WNT-T Cell Factor (TCF) Pathway Response Blocker
Hippo↓,
Akt↓, Ivermectin inhibits the Akt/mTOR signalling pathway by increasing the ubiquitination-mediated degradation of PAK1,
mTOR↓,
angioG↓, In addition, ivermectin induces the multidrug resistance protein (MDR), has potent anti-mitotic activity, targets angiogenesis and inhibits cancer stem-like cells (CSCs).
CSCs↓, Ivermectin Is an Inhibitor of CSCs
MMP↓, collapse of the mitochondrial membrane potential (ΔΨm) and the release of cytochrome c,
Cyt‑c↑,
Apoptosis↑, ivermectin induces apoptosis in glioblastoma and HeLa cells by enhancing cytochrome c release, upregulating Bax and p53 expression, downregulating Bcl-2 expression and decreasing the levels of cyclin E, cyclin D1, CDK2, CDK6 and CDK4
BAX↑,
P53↑,
Bcl-2↓,
cycE/CCNE↓,
cycD1/CCND1↓,
CDK2↓,
CDK6↓,
CDK4↓,
YAP/TEAD↓, Ivermectin Inhibits Proliferation by Inhibiting Yea-Associated Protein 1 (YAP1)
TFE3↑, Ivermectin treatment increases TFE3(Ser321) dephosphorylation, activates TFE3 nuclear translocation and stimulates activation of the TFE3 reporter in human melanoma cells
mTORC1↓, Ivermectin treatment also clearly decreases phosphorylation of the mTORC1 substrate p-70S6K, which results in induction of mTORC1 deactivation.
mitResp↓, Ivermectin Inhibits Mitochondrial Respiration
OCR↓, inhibitory effect of ivermectin on the basal oxygen consumption rate (OCR) and maximum OCR in U87, T98G
compI↓, ivermectin inhibits mitochondrial respiration by decreasing the activity of respiratory complex I enzyme
MMP↓, ivermectin decreased the mitochondrial membrane potential,
ROS↑, Consistently, obviously increased levels of ROS and mitochondrial superoxide as well as decreased ATP levels were also found in glioblastoma, HBMECs and chronic myeloid leukaemia (CML) cells treated with ivermectin
SOD2↑,
ATP↓,
eff↓, (ALCAR, a mitochondrial fuel) and N-acetyl-l-cysteine (NAC, an antioxidant) reversed the inhibitory effects of ivermectin in renal cell carcinoma (RCC) cells, which indicates that mitochondria are the target of ivermectin.
mitA↓, Ivermectin Exerts Anti-Mitotic Activity
P-gp/ABCB1↓, Ivermectin Is a P-Glycoprotein (P-Gp) Inhibitor
TumVol↓, After 10 to 42 days, treatment with ivermectin can reduced the tumour volume by more than 50%.

8022-

IVM,

Antibiotic ivermectin preferentially targets renal cancer through inducing mitochondrial dysfunction and oxidative damage

vitro+vivo,

RCC,

 xenograft mouse model.

AntiP↑, we investigated the effects and mechanism of anti-parasitic agent ivermectin in RCC
TumCP↓, ivermectin significantly inhibits proliferation and induces apoptosis in multiple RCC cell lines that represent different histological subtypes and various mutation status.
Apoptosis↑,
selectivity↑, ivermectin is significantly less or ineffective in normal kidney cells compared with RCC cells, demonstrating the preferential toxicity of ivermectin to RCC.
TumCG↓, Ivermectin also significantly inhibits RCC tumor growth in vivo.
MMP↓, ivermectin induces mitochondrial dysfunction via decreasing mitochondrial membrane potential, mitochondrial respiration and ATP production.
mitResp↓,
ATP↓,
ROS↑, As a consequence of mitochondrial dysfunction, oxidative stress and damage is detected in ivermectin treated RCC cells and xenograft mouse model.
eff↓, The rescue of ivermectin's effect by acetyl-l-Carnitine (ALCAR, a mitochondrial fuel) or antioxidant N-acetyl-l-cysteine (NAC) confirms mitochondria as the target of ivermectin in RCC cells.

8021-

IVM,

The antiparasitic agent ivermectin induces chloride-dependent membrane hyperpolarization and cell death in leukemia cells

vitro+vivo,

AML,

HL-60

NA,

lymphoma,

U937

NA,

Pca,

DU145

AntiP↑, From these screens, we identified ivermectin, a derivative of avermectin B1 that is licensed for the treatment of the parasitic infections, strongyloidiasis and onchocerciasis, but is also effective against other worm infestations.
TumCD↑, ivermectin induced cell death at low micromolar concentrations in acute myeloid leukemia cell lines and primary patient samples preferentially over normal hematopoietic cells.
selectivity↑,
TumCG↓, Ivermectin also delayed tumor growth in 3 independent mouse models of leukemia at concentrations that appear pharmacologically achievable.
i-Chl↑, Ivermectin increased intracellular chloride ion concentrations and cell size in leukemia cells.
ROS↑, Ivermectin also increased reactive oxygen species generation that was functionally important for ivermectin-induced cell death.
ChemoSen↑, Finally, ivermectin synergized with cytarabine and daunorubicin that also increase reactive oxygen species production.

8020-

IVM,

Ivermectin induces PAK1-mediated cytostatic autophagy in breast cancer

vitro+vivo,

BC,

AntiP↑, Ivermectin is a broad-spectrum antiparasitic drug that has recently been demonstrated to exhibit potent anticancer activity against colon cancer, ovarian cancer, melanoma and leukemia.
TumAuto↑, We recently found that ivermectin markedly inhibits the growth of breast cancer cells by stimulating cytostatic macroautophagy/autophagy in vitro and in vivo.
Akt↓, inhibits the AKT-MTOR signaling pathway by promoting ubiquitination-mediated degradation of PAK1 (p21 [RAC1] activated kinase 1), leading to increased autophagic flux.
mTOR↓,
PAK1↓,
selectivity↑, marked growth inhibition after 24-h treatment with ivermectin in a range of breast cancer cell lines, with no obvious effects on nontumorigenic human breast cells.

8049-

IVM,

Ivermectin Induces Cytostatic Autophagy by Blocking the PAK1/Akt Axis in Breast Cancer

vitro+vivo,

BC,

breast cancer xenografts

*AntiP↑, Ivermectin, a broad-spectrum antiparasitic drug, has recently been characterized as a potential anticancer agent due to observed antitumor effects.
AntiCan↑,
AntiTum↑,
PAK1↓, decreased P21-activated kinase 1 (PAK1) expression via the ubiquitination-mediated degradation pathway.
p‑Akt↓, decreases the phosphorylation level of Akt, resulting in the blockade of the Akt/mTOR signaling pathway.
Akt↓,
mTOR↓,
TumCG↓, In breast cancer xenografts, the ivermectin-induced cytostatic autophagy leads to suppression of tumor growth.

8044-

IVM,

Current therapeutic applications and pharmacokinetic modulations of ivermectin

Review,

Var,

*AntiP↑, Ivermectin is considered to be a wonder drug due to its broad-spectrum antiparasitic activity against both ectoparasites and endoparasites (under class of endectocide) and has multiple applications in both veterinary and human medicine
BioAv↓, Ivermectin is generally insoluble and unstable in aqueous preparations. Hence, to overcome the problem of poor water solubility and obtain a stable injectable formulation of ivermectin, several commercial preparations have been developed which use or

8237-

LCA,

Role of Licochalcone A in Potential Pharmacological Therapy: A Review

Review,

Var,

*other↝, Licorice always functions as an adjuvant drug in traditional Chinese medicine to reduce the toxicity of other medicinal herbs or enhance their pharmacological effects.
*Inflam↓, LA demonstrates various pharmacological properties, including anti-inflammation, antibacterial, antioxidant, anti-parasitic, bone protection, neuroprotection, skin protection, and blood glucose and lipid regulation.
*Bacteria↓,
*antiOx↑,
*AntiP↑,
*neuroP↑,
*glucose↝,
*lipid-P↓,
PKCδ↓, Downregulation of PKCε, p70S6K, and Akt is also described
P70S6K↓,
Akt↓,
ER Stress↑, LA induced ER stress in HepG2 cells to induce apoptosis
Apoptosis↑,
Ca+2↑, enhancing cytosolic Ca2+ release from the ER
PI3K↓, apoptosis of MCF-7 by inhibiting PI3K-Akt-mTOR signaling, thereby increasing caspase-3 activity, decreasing expression of B-cell lymphoma-2, and triggering the release of cytochrome from mitochondria into the cytoplasm
mTOR↓,
Casp3↑,
Bcl-2↓,
Cyt‑c↑,
BAX↑, upregulation of Bax expression and PARP cleavage, downregulation of Bcl-2 and Cyclin D1, and accumulation of reactive oxygen species (ROS)
cl‑PARP↑,
cycD1/CCND1↑,
ROS↑,
CHOP/DDIT3↑, CHOP expression was elevated in parallel
ERK↑, LA significantly activated ERK and p38 in A549 and H460 cells in a time-dependent manner.
p38↑,
JNK↓, LA also inhibited the activity of JNK, suppressed the expression of c-IAP1, c-IAP2, XIAP, Survivin, c-FLIPL, and RIP1, and attenuated LA-induced induction of autophagy
IAP1↓,
XIAP↓,
survivin↓,
cFLIP↓,
RIP1↓,
EGFR↓, promoted the degradation of EGFR, Met, Her2
MET↓,
HER2/EBBR2↓,
p‑4E-BP1↓, LA may inhibit the phosphorylation of 4EBP1 (Ser 65) and activate the PERK-eIF2α pathway to inhibit PD-L1 translation
PERK↑,
eIF2α↑,
PD-L1↓,
HK2↓, Hexokinase 2Â (HK2) expression was downregulated at a lower dose, attenuating glycolysis elevation and inducing apoptosis in MKN-45 and SGC7901 cells
Glycolysis↓,
Sp1/3/4↓, LA induced apoptosis via downregulating the expression of specificity protein 1 (Sp1), upregulating Bax, Bid, Bcl-xl, caspase-3, and PARP cleavage with doses of 10–40 μM
FasL↑, LA induced apoptosis in KB cells, relying on activation of caspase-dependent factor associated suicide ligand (FasL) mediated death receptor pathway.
MMP↓, reducing mitochondrial membrane potential and inhibiting ATP production in vitro
ATP↓,
TumAuto↑, The literature also showed that LA induced apoptosis and autophagy in SiHa
WEE1↑, LA blocked the cell cycle in HepG2 cells by increasing the expression of Weel, P21, Cyclin D1, and JNK1 and decreasing the expression of Survivin, Cyclin B1, and CDK1 using doses of 30–70 μM
P21↑,
CDK1↓,
TumCCA↑,
TumCMig↓, LA exhibited the ability to inhibit migration and invasion of A549 and H460 cells at relatively lower doses (2–20 μM)
TumCI↓,
ABCG2↓, downregulating the expression of breast cancer resistance protein (BCRP)
HSP90↓, LA also reduced Hsp90 activity in gefitinib-resistant NSCLC cells (H1975) via binding to the N-terminal ATP binding site of Hsp90 to reduce drug resistance
T-Cell↑, LA (40 mg/kg) to C3H/HeN mice bearing UM-UC-3 cells enhanced the activity of cytotoxic T lymphocytes and counts of CD4+ CD25+ Foxp3+ T regulatory T cells. Thus, LA might treat bladder cancer by modulating the tumor immune microenvironment
CD4+↑,
CD25+↑,
FOXP3↑,
Imm↝,
*Inflam↓, LA demonstrates anti-inflammatory activity via interaction with MAPK, NF-κB, NLRP3, and Nrf2 signaling in the acute lung, kidney, and liver injury (acute inflammation) and arthritis and asthma
*NF-kB↓,
*NRF2↑,
*AntiArt↑,

8253-

LCA,

Licochalcone A, a natural chalconoid isolated from Glycyrrhiza inflata root, induces apoptosis via Sp1 and Sp1 regulatory proteins in oral squamous cell carcinoma

in-vitro,

SCC,

HSC4

*AntiTum↑, antitumor, anti-angiogenesis, antiparasitic, anti-oxidant, antibacterial and anti-inflammatory effects.
*angioG↓,
*AntiP↑,
*antiOx↑,
*Bacteria↓,
*Inflam↓,
tumCV↓, LCA inhibited OSCC cell (HN22 and HSC4) growth in a concentration- and time-dependent manner.
Sp1/3/4↓, Mechanistically, it was mediated via downregulation of specificity protein 1 (Sp1) expression and subsequent regulation of Sp1 downstream proteins such as p27, p21, cyclin D1, Mcl-1 and survivin.
p27/CDKN1B↑, Cell cycle arrest proteins such as p27 and p21 were elevated in HN22 (Fig. 3A) and HSC4 (Fig. 3B) by LCA treatment while cell proliferation and survival-related proteins like cyclin D1, Mcl-1 and survivin were diminished
P21↑,
cycD1/CCND1↓,
Mcl-1↓,
survivin↓,
Apoptosis↑, LCA induces apoptosis in OSCCs.

8206-

LCA,

Licochalcone A-induced human gastric cancer BGC-823 cells apoptosis by regulating ROS-mediated MAPKs and PI3K/AKT signaling pathways

in-vivo,

GC,

BGC-823

KM mice in vivo

ROS?, LA increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding and activation of caspase-3, and cleavage of poly-ADP-ribose polymerase (PARP).
Casp3↑,
cl‑PARP↑,
eff↓, Inhibition of ROS generation by N-acetylcysteine (NAC) significantly prevented LA-induced apoptosis.
ERK↑, LA caused the activation of ERK, JNK, and p38 MAPK in BGC-823 cells.
JNK↑,
MAPK↑,
AntiP↑, Licochalcone A (LA, Fig. 1) is a flavonoid extracted from licorice root and has antiparasitic and anti-tumor activities
AntiTum↑,
TumCP↓, LA inhibited cell proliferation in BGC cells
selectivity↑, LA significantly suppressed the viability of human gastric cancer cells, with significantly lower toxicity against normal human gastric cells,
GSH/GSSG↓, GSH/GSSG ratio decreased obviously, accompanied with MDA (Malondialdehyde, a marker for oxidative stress, results from lipid peroxidation of polyunsaturated fatty acids.
MDA↑,
lipid-P↑,
PI3K↓, The data indicated that the inhibition of PI3K/AKT signaling cascade by LA leaded to the suppression of cell proliferation in human gastric cancer BGC cells.
Akt↓,

8208-

LCA,

Licochalcone A inhibits PI3K/Akt/mTOR signaling pathway activation and promotes autophagy in breast cancer cells

in-vitro,

BC,

MCF7

*Inflam↓, Licochalcone A possesses anti-inflammatory, anticancer, anti-bacterial, anti-malarial and anti-parasitic activities.
*AntiCan↑,
*AntiP↑,
LC3II↑, Licochalcone A treatment activated the LC3-II signaling pathway while suppressing the phosphoinositide 3-kinase (PI3K)/RAC-α serine-threonine-protein kinase (Akt)/mammalian target of rapamycin (mTOR) signaling pathway.
PI3K↓,
Akt↓,
mTOR↓,
Casp3↑, Licochalcone A significantly increased caspase-3 activity and significantly decreased B-cell lymphoma-2 expression.
Bcl-2↓,
TumAuto↑, results from the present study indicate that Licochalcone A inhibits PI3K/Akt/mTOR activation, and promotes autophagy and apoptosis in MCF-7 cells.
Apoptosis↑,
tumCV?, At 24 h, 50 or 100 µM Licochalcone A significantly decreased cell viability compared with the 0 µM control group

8229-

LCA,

Licochalcone A: a review of its pharmacology activities and molecular mechanisms

Review,

Nor,

*Inflam↓, Lico A mitigates LPS-induced effects by inhibiting inflammatory cytokine production and NO through NF-κB pathway suppression.
*NO↓,
*NF-kB↓,
*TAC↑, Lico A enhances the activity of antioxidant enzymes and protects against oxidative damage and cell death via ERK and Akt pathways
Apoptosis?, Lico A exhibits significant anti-tumor effects (Kang et al., 2017; Wu et al., 2017; Chen et al., 2018a), including the induction of apoptosis in cancer cells, regulation of the cell cycle, inhibition of tumor invasion and metastasis, and suppression
TumCCA↑,
TumCI↓,
TumMeta↓,
TumCP↓,
MAPK↓, Lico A acts to inhibit this process by restraining cell migration, modulating E-cadherin and vimentin expression, and blocking MAPK and AKT signaling pathways (
Akt↓,
IL6↓, suppressing angiogenesis factors such as IL-6, IL-8, and the VEGFR-2 signaling pathway
IL8↓,
VEGFR2/KDR/Flk1↓,
LC3II↑, MCF-7 20–100 Activate the LC3-II signaling pathway while suppressing the PI3K/Akt/mTOR/signaling pathway
PI3K↓,
mTOR↓,
mtDam↑, Lymphoma T24 20–80 Induce mitochondrial dysfunction, decreased mitochondrial membrane potential
MMP↓,
*NRF2↑, Research has uncovered that Lico A’s anti-arthritis effects depend on the activation of the Keap1-Nrf2 signaling pathway through p62 phosphorylation at the Ser349 site
*PGE2↓, Skin inflammation HT1080/HDF post-shave irritation model Decreased NF-κB and PGE2 secretion
*Obesity↓, Research has shown that Lico A treatment in high-fat diet (HFD)-induced obese mice reduces body weight and decreases inguinal and epididymal adipose tissue compared to HFD-treated mice.
*SIRT1↑, Lico A’s specific lipid-lowering mechanism involves activating the SIRT1/AMPK pathway, reducing fatty acid synthesis, and enhancing lipolysis and beta-oxidation in hepatocytes
*AMPK↑,
*AntiFungal↑, Lico A exhibits substantial antifungal activity against Candida albicans, inhibiting biofilm formation by 35%–60%, and suppressing yeast-hyphal transformation and protease secretion
*AntiP↑, Additionally, Lico A reduces the total number of Schistosoma mansoni eggs, likely by increasing ROS production and inducing the death of adult Schistosoma mansoni
*BMD↑, Lico A administration restores or protects bone mass in disease states
*GastroP↑, ico A could promote intestinal epithelial renewal to exert intestinal protective effect

8203-

LGE,

Eug,

Citral and eugenol modulate DNA damage and pro-inflammatory mediator genes in murine peritoneal macrophages

in-vitro,

Nor,

 LPS-activated cells,

*Inflam↓, Citral and eugenol have been broadly studied because of their anti-inflammatory, antioxidant and antiparasitic potentials.
*antiOx↑,
*AntiP↑,
*Dose↝, In this study, the effects of citral (25, 50 and 100 µg/mL) and eugenol (0.31, 0.62, 1.24 and 2.48 µg/mL) on the expression (RT-PCR) of the pro-inflammatory mediator genes NF-κB1, COX-2 and TNF-α were evaluated in mouse peritoneal macrophages
*toxicity↝, but the use of these compounds must be viewed with caution because they are also able to induce primary DNA lesions.
*COX2/PTGS2↓, However, in LPS-activated cells, citral induced the hypoexpression of COX-2 (100 µg/mL) and TNF-α (50 and 100 µg/mL).
*TNF-α↓,

Showing Research Papers: 1 to 18 of 18

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1, AntiP↑, 14, Stroke↝, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3, lipid-P↓, 1, NRF2↑, 2, TAC↑, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1, glucose↝, 1, SIRT1↑, 1,

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1, NO↓, 1,

Barriers & Transport(tgid=15) ⓘ

GastroP↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1, Inflam↓, 7, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,

Functional Outcomes(tgid=23) ⓘ

AntiCan↓, 1, AntiCan↑, 1, AntiDiabetic↑, 1, AntiTum↑, 1, cardioP↑, 1, neuroP↑, 2, Obesity↓, 1, toxicity↓, 1, toxicity↑, 1, toxicity↝, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 2,
Total Targets: 34

Scientific Paper Hit Count for: AntiP, antiparasitic

12 Ivermectin
5 Licochalcone A
1 Lemongrass Extract/Citral
1 Eugenol

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#:1749  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

AntiP Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

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

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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