Ivermectin / ROS Cancer Research Results

IVM, Ivermectin: Click to Expand ⟱

Features:

Ivermectin — a semisynthetic avermectin-derived macrocyclic lactone and prescription antiparasitic drug, commonly abbreviated IVM and marketed orally as Stromectol. It is formally an anthelmintic/antiparasitic agent derived from avermectins originally isolated from Streptomyces avermitilis. Its established therapeutic action is activation/modulation of invertebrate glutamate-gated chloride channels, producing paralysis and death of susceptible parasites. In oncology, ivermectin is an investigational drug-repurposing candidate rather than an approved anticancer therapy. Preclinical cancer models report multiple effects including PAK1/AKT/mTOR suppression, mitochondrial dysfunction and oxidative stress, WNT-TCF inhibition, Hippo/YAP1 suppression, chloride-dependent cytotoxicity, and immunogenic cell-death/immune modulation.

Primary mechanisms (ranked):

PAK1 degradation with downstream AKT/mTOR suppression and induction of cytostatic/autophagic programs, particularly demonstrated in breast-cancer models.
Mitochondrial dysfunction with ↓ mitochondrial membrane potential, ↓ respiration and ↓ ATP, producing secondary ROS accumulation, oxidative damage and intrinsic apoptosis in several cancer models.
WNT/β-catenin-TCF pathway suppression, reducing WNT-dependent transcription, proliferation, cyclin D1 and cancer-cell growth in responsive models.
Hippo/YAP1 signaling suppression, including ↓ YAP1 expression/nuclear accumulation and ↓ downstream CTGF in susceptible tumor models.
ATP/P2X4/P2X7 signaling modulation and immunogenic cancer-cell death, with increased antitumor T-cell activity and reduced immunosuppressive populations in preclinical breast-cancer models; this provides the rationale for current immune-checkpoint-inhibitor combination trials.
Chloride-channel-associated membrane effects, including chloride-dependent hyperpolarization/cytotoxicity demonstrated in leukemia cells.
Importin α/β-mediated nuclear transport inhibition, potentially affecting transcription factors and other cargo; mechanistically established but tumor relevance varies substantially by model.
JAK/STAT, glycolytic and other metabolic suppression in selected tumor models; these are context-dependent rather than universal ivermectin mechanisms.

Bioavailability / PK relevance: Oral ivermectin is highly lipophilic and poorly water-soluble. After a fasting 12-mg oral dose, reported mean peak plasma concentrations are approximately 31–47 ng/mL at about 4 hours, with a plasma half-life of approximately 18 hours. It is primarily metabolized by CYP3A4 and eliminated predominantly in feces. A high-fat meal can increase systemic bioavailability approximately 2.5-fold. P-glycoprotein-mediated efflux is important in limiting CNS exposure; disruption or inhibition of this protective transport mechanism can increase neurotoxicity risk. Drug interactions and altered hepatic metabolism become particularly important when considering nonstandard high or repeated oncology dosing.

In-vitro vs systemic exposure relevance: A major translational limitation is the exposure gap. Standard antiparasitic dosing produces peak circulating concentrations in the tens of ng/mL, corresponding to only roughly 0.04–0.06 µM, whereas many direct anticancer experiments use approximately 2.5–20 µM or higher ivermectin. Thus, common in-vitro anticancer concentrations can exceed conventional human systemic exposure by tens to several hundred-fold. Some tumor-selective or immune-modulatory effects may occur at lower exposures, and oncology trials are testing repeated dosing, but direct extrapolation of micromolar cell-culture cytotoxicity to standard oral dosing is not justified.

Clinical evidence status: Approved antiparasitic; oncology investigational. The anticancer evidence remains predominantly preclinical, with substantial cell-culture, organoid, xenograft and immunologic evidence but very limited human efficacy data. A Phase I/II study of ivermectin plus pembrolizumab or balstilimab in metastatic triple-negative breast cancer is recruiting, and a separate randomized Phase II ICONIC study is planned to evaluate ivermectin with standard immune-checkpoint inhibition in solid tumors. No completed large randomized controlled trial has established ivermectin as an effective cancer treatment, and it has no FDA or Health Canada oncology indication.

Ivermectin Mechanistic Profile

Rank	Pathway / Axis	Cancer Cells	Normal Cells	Primary Effect	Notes / Interpretation
1	PAK1 / AKT / mTOR	PAK1 ↓ AKT ↓ mTOR ↓ Autophagic flux ↑	↔ / not established	Cytostatic autophagy and reduced proliferation	Strong mechanistic evidence in breast-cancer models; ivermectin promotes ubiquitination-mediated degradation of PAK1 with subsequent suppression of AKT/mTOR signaling.
2	Mitochondrial bioenergetics	Mitochondrial membrane potential ↓ Mitochondrial respiration ↓ ATP ↓	↔ / ↓ (high exposure)	Bioenergetic failure and apoptosis	Demonstrated particularly in renal, colorectal and esophageal cancer models. Preferential effects over corresponding normal cells have been reported in some models but should not be generalized to all tissues.
3	Mitochondrial ROS and oxidative damage	ROS ↑ (dose-dependent)	↔ / ↑ (high exposure)	Oxidative stress and intrinsic apoptosis	ROS is principally a downstream consequence of mitochondrial dysfunction rather than a universal primary molecular target. NAC or mitochondrial metabolic rescue can attenuate ivermectin cytotoxicity in several experimental systems.
4	WNT / β-catenin / TCF	WNT-TCF transcription ↓ β-catenin signaling ↓ CCND1 ↓	↔ / not established	Reduced proliferation and WNT-dependent tumor growth	Well-characterized preclinical repurposing mechanism, particularly relevant to tumors dependent on canonical WNT-TCF signaling.
5	Hippo / YAP1 / CTGF	YAP1 ↓ YAP1 nuclear localization ↓ CTGF ↓ (model-dependent)	↔ / not established	Reduced oncogenic transcription and proliferation	Demonstrated in gastric and other YAP-dependent cancer models. Sensitivity is heterogeneous, and recent organoid work indicates substantial tumor-to-tumor and time-dependent variation.
6	ATP / P2X4 / P2X7 immune signaling	Immunogenic cell death ↑	Antitumor T-cell activity ↑ Immunosuppressive populations ↓ (model-dependent)	Conversion toward an immunologically active tumor microenvironment	Preclinical breast-cancer studies provide the rationale for combining ivermectin with PD-1 pathway inhibition. Human therapeutic benefit remains unproven.
7	Chloride-dependent membrane signaling	Intracellular Cl⁻ ↑ Membrane hyperpolarization ↑ Cell death ↑	Lower effect (model-dependent)	Preferential leukemia-cell cytotoxicity	One of the earliest experimentally demonstrated anticancer mechanisms. Evidence is strongest in leukemia and should not be assumed to be dominant in solid tumors.
8	JAK / STAT signaling	JAK2 ↓ p-STAT3 ↓ p-STAT5 ↓ (model-dependent)	↔ / not established	Reduced survival and metabolic signaling	Demonstrated in selected models including glioma; not established as a universal ivermectin target across cancer types.
9	Glycolytic metabolism	GLUT4 ↓ HK2 ↓ PFK1 ↓ Pyruvate ↓ ATP ↓ (model-dependent)	↔ / ↓ (high concentration only)	Reduced glycolytic capacity and enhanced metabolic stress	Strongly demonstrated in particular glioma models through GLUT4/JAK/STAT signaling, but insufficient evidence supports treating glycolysis as a universal primary ivermectin mechanism.
10	Intrinsic apoptosis	Bax ↑ Bcl-2 ↓ Caspase activity ↑ PARP cleavage ↑	↔ / ↑ (high exposure)	Programmed tumor-cell death	Common downstream phenotype following mitochondrial dysfunction, ROS accumulation and signaling disruption.
11	Importin α / β nuclear transport	Importin-dependent nuclear transport ↓	↓ (exposure-dependent)	Reduced nuclear localization of susceptible cargo	Biochemically important ivermectin activity, but it is not cancer-cell-specific and its contribution to antitumor effects varies by substrate and tumor context.
12	HIF hypoxia signaling	HIF-1α nuclear localization ↓ HIF transcription ↓ (model-dependent)	↓ (context-dependent)	Reduced cellular hypoxia-response transcription	Likely linked partly to importin α/β inhibition. Relevant in hypoxic models but not sufficiently universal to rank as a core ivermectin anticancer mechanism.
13	Cancer stemness and invasion	Stemness ↓ Migration ↓ Invasion ↓ (model-dependent)	↔ / not established	Reduced aggressive tumor phenotype	Reported across several preclinical systems and probably reflects convergence of WNT, YAP, AKT and related pathways rather than a single direct target.
14	NRF2 antioxidant response	↔ / context-dependent	↔ / context-dependent	Not established as a core ivermectin mechanism	Evidence is insufficient to assign a consistent ivermectin-induced NRF2 direction across cancers. It should not currently be presented as a standard ivermectin pathway.
15	Clinical Translation Constraint	Effective experimental exposure often exceeds standard human exposure	Neurotoxicity and systemic toxicity risk ↑ with excessive exposure	Limits translation of direct in-vitro cytotoxicity	Standard oral dosing produces approximately 0.04–0.06 µM peak plasma concentrations, whereas many cancer-cell experiments use several µM. CYP3A4 metabolism, food-dependent exposure, P-glycoprotein-mediated CNS protection, concomitant drugs and repeated high dosing are important clinical constraints. Current oncology studies are investigational and efficacy remains unconfirmed.

ROS, Reactive Oxygen Species: Click to Expand ⟱

Source: HalifaxProj (inhibit)

Type:

Reactive oxygen species (ROS) are highly reactive molecules that contain oxygen and can lead to oxidative stress in cells. They play a dual role in cancer biology, acting as both promoters and suppressors of cancer.
ROS can cause oxidative damage to DNA, leading to mutations that may contribute to cancer initiation and progression. So normally you want to inhibit ROS to prevent cell mutations.
However excessive ROS can induce apoptosis (programmed cell death) in cancer cells, potentially limiting tumor growth. Chemotherapy typically raises ROS.
-mitochondria is the main source of reactive oxygen species (ROS) (and the ETC is heavily related)
ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target

"Reactive oxygen species (ROS) are two electron reduction products of oxygen, including superoxide anion, hydrogen peroxide, hydroxyl radical, lipid peroxides, protein peroxides and peroxides formed in nucleic acids 1. They are maintained in a dynamic balance by a series of reduction-oxidation (redox) reactions in biological systems and act as signaling molecules to drive cellular regulatory pathways."
"During different stages of cancer formation, abnormal ROS levels play paradoxical roles in cell growth and death 8. A physiological concentration of ROS that maintained in equilibrium is necessary for normal cell survival. Ectopic ROS accumulation promotes cell proliferation and consequently induces malignant transformation of normal cells by initiating pathological conversion of physiological signaling networks. Excessive ROS levels lead to cell death by damaging cellular components, including proteins, lipid bilayers, and chromosomes. Therefore, both scavenging abnormally elevated ROS to prevent early neoplasia and facilitating ROS production to specifically kill cancer cells are promising anticancer therapeutic strategies, in spite of their contradictoriness and complexity."
"ROS are the collection of derivatives of molecular oxygen that occur in biology, which can be categorized into two types, free radicals and non-radical species. The non-radical species are hydrogen peroxide (H 2O 2 ), organic hydroperoxides (ROOH), singlet molecular oxygen ( 1 O 2 ), electronically excited carbonyl, ozone (O3 ), hypochlorous acid (HOCl, and hypobromous acid HOBr). Free radical species are super-oxide anion radical (O 2•−), hydroxyl radical (•OH), peroxyl radical (ROO•) and alkoxyl radical (RO•) [130]. Any imbalance of ROS can lead to adverse effects. H2 O 2 and O 2 •− are the main redox signalling agents. The cellular concentration of H2 O 2 is about 10−8 M, which is almost a thousand times more than that of O2 •−".
"Radicals are molecules with an odd number of electrons in the outer shell [393,394]. A pair of radicals can be formed by breaking a chemical bond or electron transfer between two molecules."

Recent investigations have documented that polyphenols with good antioxidant activity may exhibit pro-oxidant activity in the presence of copper ions, which can induce apoptosis in various cancer cell lines but not in normal cells. "We have shown that such cell growth inhibition by polyphenols in cancer cells is reversed by copper-specific sequestering agent neocuproine to a significant extent whereas iron and zinc chelators are relatively ineffective, thus confirming the role of endogenous copper in the cytotoxic action of polyphenols against cancer cells. Therefore, this mechanism of mobilization of endogenous copper." > Ions could be one of the important mechanisms for the cytotoxic action of plant polyphenols against cancer cells and is possibly a common mechanism for all plant polyphenols. In fact, similar results obtained with four different polyphenolic compounds in this study, namely apigenin, luteolin, EGCG, and resveratrol, strengthen this idea.
Interestingly, the normal breast epithelial MCF10A cells have earlier been shown to possess no detectable copper as opposed to breast cancer cells [24], which may explain their resistance to polyphenols apigenin- and luteolin-induced growth inhibition as observed here (Fig. 1). We have earlier proposed [25] that this preferential cytotoxicity of plant polyphenols toward cancer cells is explained by the observation made several years earlier, which showed that copper levels in cancer cells are significantly elevated in various malignancies. Thus, because of higher intracellular copper levels in cancer cells, it may be predicted that the cytotoxic concentrations of polyphenols required would be lower in these cells as compared to normal cells."

Majority of ROS are produced as a by-product of oxidative phosphorylation, high levels of ROS are detected in almost all cancers.
-It is well established that during ER stress, cytosolic calcium released from the ER is taken up by the mitochondrion to stimulate ROS overgeneration and the release of cytochrome c, both of which lead to apoptosis.

Note: Products that may raise ROS can be found using this database, by:
Filtering on the target of ROS, and selecting the Effect Direction of ↑

Targets to raise ROS (to kill cancer cells):
• NADPH oxidases (NOX): NOX enzymes are involved in the production of ROS.
    -Targeting NOX enzymes can increase ROS levels and induce cancer cell death.
    -eNOX2 inhibition leads to a high NADH/NAD⁺ ratio which can lead to increased ROS
• Mitochondrial complex I: Inhibiting can increase ROS production
• P53: Activating p53 can increase ROS levels(by inducing the expression of pro-oxidant genes)
• Nrf2 inhibition: regulates the expression of antioxidant genes. Inhibiting Nrf2 can increase ROS levels
• Glutathione (GSH): an antioxidant. Depleting GSH can increase ROS levels
• Catalase: Catalase converts H2O2 into H2O+O. Inhibiting catalase can increase ROS levels
• SOD1: converts superoxide into hydrogen peroxide. Inhibiting SOD1 can increase ROS levels
• PI3K/AKT pathway: regulates cell survival and metabolism. Inhibiting can increase ROS levels
• HIF-1α inhibition: regulates genes involved in metabolism and angiogenesis. Inhibiting HIF-1α can increase ROS
• Glycolysis: Inhibiting glycolysis can increase ROS levels • Fatty acid oxidation: Cancer cells often rely on fatty acid oxidation for energy production.
-Inhibiting fatty acid oxidation can increase ROS levels
• ER stress: Endoplasmic reticulum (ER) stress can increase ROS levels
• Autophagy: process by which cells recycle damaged organelles and proteins.
-Inhibiting autophagy can increase ROS levels and induce cancer cell death.
• KEAP1/Nrf2 pathway: regulates the expression of antioxidant genes.
    -Inhibiting KEAP1 or activating Nrf2 can increase ROS levels and induce cancer cell death.
• DJ-1: regulates the expression of antioxidant genes. Inhibiting DJ-1 can increase ROS levels
• PARK2: regulates the expression of antioxidant genes. Inhibiting PARK2 can increase ROS levels
• SIRT1 inhibition:regulates the expression of antioxidant genes. Inhibiting SIRT1 can increase ROS levels
• AMPK activation: regulates energy metabolism and can increase ROS levels when activated.
• mTOR inhibition: regulates cell growth and metabolism. Inhibiting mTOR can increase ROS levels
• HSP90 inhibition: regulates protein folding and can increase ROS levels when inhibited.
• Proteasome: degrades damaged proteins. Inhibiting the proteasome can increase ROS levels
• Lipid peroxidation: a process by which lipids are oxidized, leading to the production of ROS.
    -Increasing lipid peroxidation can increase ROS levels
• Ferroptosis: form of cell death that is regulated by iron and lipid peroxidation.
    -Increasing ferroptosis can increase ROS levels
• Mitochondrial permeability transition pore (mPTP): regulates mitochondrial permeability.
    -Opening the mPTP can increase ROS levels
• BCL-2 family proteins: regulate apoptosis and can increase ROS levels when inhibited.
• Caspase-independent cell death: a form of cell death that is regulated by ROS.
    -Increasing caspase-independent cell death can increase ROS levels
• DNA damage response: regulates the repair of DNA damage. Increasing DNA damage can increase ROS
• Epigenetic regulation: process by which gene expression is regulated.
    -Increasing epigenetic regulation can increase ROS levels

-PKM2, but not PKM1, can be inhibited by direct oxidation of cysteine 358 as an adaptive response to increased intracellular reactive oxygen species (ROS)

ProOxidant Strategy:(inhibit the Mevalonate Pathway (likely will also inhibit GPx)
-HydroxyCitrate (HCA) found as supplement online and typically used in a dose of about 1.5g/day or more
-Atorvastatin typically 40-80mg/day, -Dipyridamole typically 200mg 2x/day Combined effect research
-Lycopene typically 100mg/day range (note debatable as it mainly lowers NRF2)

Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy

ROS-Inducing Interventions in Cancer — Canonical + Mechanistic Reference
-generated from AI and Cancer database
ROS rating:  +++ strong | ++ moderate | + weak | ± mixed | 0 none
NRF2:        ↓ suppressed | ↑ activated | ± mixed | 0 none
Conditions:  [D] dose  [Fe] metal  [M] metabolic  [O₂] oxygen
             [L] light [F] formulation [T] tumor-type [C] combination


Item  ROS↑  NRF2  Condition  Mechanism Class  Remarks  

ROS">Piperlongumine
+++  ↓  [D][T]  ROS-dominant
Selective <span class="wphighlight">ROS</span> stressor, Prevents compensatory upregulation of NRF2, ie GSH↓



ROS">Shikonin
+++ ↓/± [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + glycolysis + GPX4 inhibition



ROS">Vitamin K3 (menadione)
+++ ↓ [D] ROS-dominant
Quinone redox cycler; toxicity limits use



ROS">Copper (ionic / nano)
+++ ↓ [Fe][F] ROS-dominant
Fenton-type redox chemistry



ROS">Sodium Selenite
+++ ↓ [D] ROS-dominant
Pro-oxidant, depletes GSH



ROS">Juglone
+++ ↓ [D] ROS-dominant
Strong quinone <span class="wphighlight">ROS</span> chemistry



ROS">Auranofin
+++ ↓ [D] ROS-dominant
TrxR inhibition → redox collapse



ROS">Photodynamic Therapy (PDT)
+++ 0 [L][O₂] ROS-dominant
Singlet oxygen is core cytotoxic mechanism



ROS">Radiotherapy / Radiation
+++ 0 [O₂] ROS-dominant
DNA damage largely via <span class="wphighlight">ROS</span>



ROS">Doxorubicin
+++ ↓ [D] ROS-dominant
Chemo; redox cycling + mitochondrial <span class="wphighlight">ROS</span>



ROS">Cisplatin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> contributes to DNA/protein damage



ROS">Salinomycin
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated CSC toxicity



ROS">Artemisinin / DHA
++ ↓ [Fe][T] ROS-dominant
Iron-activated radical generation



ROS">Sulfasalazine
++ ↓ [C][T] ROS-dominant
Ferroptosis; xCT inhibition → lipid <span class="wphighlight">ROS</span>



ROS">FMD / fasting
++ ↓ [M][C][O₂] ROS-dominant
Metabolic stress → mitochondrial <span class="wphighlight">ROS</span>



ROS">Vitamin C (pharmacologic)
++ ↓ [Fe][D] ROS-dominant
Extracellular H₂O₂ at high dose



ROS">Silver nanoparticles
++ ± [F][D] ROS-dominant
<span class="wphighlight">ROS</span> common; selectivity unreliable



ROS">Gambogic acid
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Parthenolide
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span> + NF-κB suppression



ROS">Plumbagin
++ ↓ [D] ROS-dominant
Quinone <span class="wphighlight">ROS</span> driver



ROS">Allicin
++ ↓ [D] ROS-dominant
Thiol-reactive oxidative stress



ROS">Ashwagandha (Withaferin A)
++ ↓ [D][T] ROS-dominant
<span class="wphighlight">ROS</span>-mediated apoptosis



ROS">Berberine
++ ↓ [D][M] ROS-dominant
Mitochondrial <span class="wphighlight">ROS</span> induction



ROS">PEITC
++ ↓ [D][C] ROS-dominant
GSH depletion + <span class="wphighlight">ROS</span>



ROS">Methionine restriction
+ ↓ [M][C][T] ROS-secondary
Redox vulnerability increased; <span class="wphighlight">ROS</span> indirect



ROS">DCA
+ ± [M][T] ROS-secondary
<span class="wphighlight">ROS</span> via forced OXPHOS



ROS">Capsaicin
+ ± [D][T] ROS-secondary
Ca²⁺ stress → <span class="wphighlight">ROS</span>



ROS">Galloflavin
+ 0 [D] ROS-secondary
<span class="wphighlight">ROS</span> not primary driver



ROS">Piperine
+ ± [D][F] ROS-secondary
Weak <span class="wphighlight">ROS</span> induction



ROS">Propyl gallate
+ ↓ [D] ROS-secondary
Pro-oxidant at high dose



ROS">Scoulerine
+ ? [D][T] ROS-secondary
Sparse <span class="wphighlight">ROS</span> data



ROS">Thymoquinone
± ± [D][T] Dual redox
Antioxidant ↔ pro-oxidant switch



ROS">Emodin
± ± [D][T] Dual redox
Not cancer-exclusive



ROS">Alpha-lipoic acid (ALA)
± ↑ [D][M] NRF2-dominant
Antioxidant at low dose



ROS">Curcumin
± ↑/↓ [D][F] NRF2-dominant
Hormetic redox behavior



ROS">EGCG
± ↑/↓ [D][O₂] NRF2-dominant
Auto-oxidation artifacts common



ROS">Quercetin
± ↑/↓ [D][Fe] NRF2-dominant
GSH-dependent cycling



ROS">Resveratrol
± ↑ [D][M] NRF2-dominant
<span class="wphighlight">ROS</span> only at high dose



ROS">Sulforaphane
± ↑↑ [D] NRF2-dominant
Strong NRF2 activator



ROS">Lycopene
0 ↑ — Antioxidant
Consistently antioxidant



ROS">Rosmarinic acid
0 ↑ — Antioxidant
Primarily antioxidant



ROS">Citrate
0 0 — Neutral
Metabolic; not a <span class="wphighlight">ROS</span> agent

Scientific Papers found: Click to Expand⟱

8035-

IVM,

Ivermectin and non-parasitic disorders: An update

Review,

Var,

Review,

AD,

Review,

Stroke,

*AntiP↑, angioG↓, *AntiCan↓, mtDam↑, Apoptosis↑, necrosis↑, TumAuto↑, ROS↑, *neuroP↑, *Stroke↝, *cardioP↑,

8036-

IVM,

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

in-vitro,

ESCC,

KYSE-30

*AntiP↑, AntiTum↑, ER Stress↑, TumAuto↑, ATF4↑, CHOP/DDIT3↝, TumCG↓, PERK↑, ROS↑, *toxicity↓, Ca+2↑,

8038-

IVM,

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

in-vitro,

PC,

*AntiP↑, AntiTum↑, ChemoSen↑, TumCP↓, TumCCA↑, cycD1/CCND1↓, mTOR↓, STAT3↑, Apoptosis↑, mtDam↑, ROS↑, MMP↓, OCR↓, MitoP↓,

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↑, TumCD↑, ROS↑, mtDam↑, Apoptosis↑, MitoP↑, TumAuto↑, p‑Akt↓, p‑mTOR↓, LC3II↑, Beclin-1/ATG6↑, ATG5↑, PINK1↑, PARK2↑, tumCV↓, MDA↑, SOD↑, Catalase↑, eff↓, MMP↓, BAX↑, cl‑Casp3↑, cl‑Casp9↑, cl‑PARP↑, Cyt‑c↑, Bcl-2↓, proCasp3↓, Bax:Bcl2↑, eff↑, *AntiP↑, *Inflam↓, *AntiDiabetic↑, *AntiViral↑, BBB∅, toxicity↝,

8040-

IVM,

Ivermectin, a potential anticancer drug derived from an antiparasitic drug

Review,

Var,

Akt↓, mTOR↓, TumAuto↑, TumCP↓, TumCCA↑, Wnt↓, YAP/TEAD↓, MMP↓, mitResp↓, ATP↓, eff↓, eff↑, ROS↑, ChemoSen↑, PAK1↓, MAPK↓, EMT↓, Beclin-1/ATG6↑, ATG5↑, CSCs↓, STAT3↝, P-gp/ABCB1↓, MDR1↓, HSP27↓, Chl↑, TFE3↑,

8045-

IVM,

Ivermectin induces cell cycle arrest and apoptosis of HeLa cells via mitochondrial pathway

in-vitro,

Cerv,

HeLa

tumCV↓, TumCCA↑, DNA-PK↑, ChrMod↝, MMP↓, Bax:Bcl2↑, Cyt‑c↓, Casp9↑, Casp3↑, ROS↑, TumCMig↓,

8047-

IVM,

The multitargeted drug ivermectin: from an antiparasitic agent to a repositioned cancer drug

Review,

Var,

Half-Life↝, MDR1↓, P-gp/ABCB1↓, mtDam↑, ROS↑, OCR↓, compI↓, MMP↓, mt-SOD↑, ATP↓, p‑Akt↓, p‑mTOR↓, eff↓, ICD↑, TumAuto↑, PAK1↓, Wnt↓, TCF↓, Nanog↓, SOX2↓, CSCs↓, CD44↓, CD24↓, Dose↝,

8025-

IVM,

Ivermectin has New Application in Inhibiting Colorectal Cancer Cell Growth

in-vitro,

CRC,

SW480

in-vivo,

CRC,

HCT116

*AntiP↓, *Inflam↓, *AntiViral↑, AntiTum↑, TumCP↓, Apoptosis↑, Casp3↑, Casp7↑, BAX↑, cl‑PARP↑, Bcl-2↓, mt-ROS↑, eff↓, Dose↝, TumCCA↑,

1175-

IVM,

PDT,

Drug induced mitochondria dysfunction to enhance photodynamic therapy of hypoxic tumors

in-vitro,

Var,

Hypoxia↓, mitResp↓, ROS↑,

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↑, TumCD↑, selectivity↑, TumCG↓, i-Chl↑, ROS↑, ChemoSen↑,

8022-

IVM,

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

vitro+vivo,

RCC,

 xenograft mouse model.

AntiP↑, TumCP↓, Apoptosis↑, selectivity↑, TumCG↓, MMP↓, mitResp↓, ATP↓, ROS↑, eff↓,

8024-

IVM,

Ivermectin induces apoptosis of esophageal squamous cell carcinoma via mitochondrial pathway

vitro+vivo,

ESCC,

KYSE-30

 nude mice model

in-vitro,

ESCC,

NE3

TumCP↓, mtDam↑, Apoptosis↑, ROS↑, NF-kB↓, Bax:Bcl2↑, LDH↝, TumCCA↑, cl‑Casp9↑, cl‑Casp3↑, cl‑PARP↑, eff↓,

8034-

IVM,

doxoR,

Synergistic potential of Ivermectin and doxorubicin in oral squamous cell carcinoma: an in vitro investigation

in-vitro,

Oral,

tumCV↓, selectivity↑, TumCCA↑, Apoptosis↓, BAX↑, Casp3↑, P53↑, Bcl-2↓, Ki-67↓, IL6↓, ROS↑, mtDam↑,

8027-

IVM,

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

Review,

Var,

*AntiP↑, TumCD↑, PAK1↑, TumAuto↑, Casp↑, ICD↑, TCF↝, Hippo↓, Akt↓, mTOR↓, angioG↓, CSCs↓, MMP↓, Cyt‑c↑, Apoptosis↑, BAX↑, P53↑, Bcl-2↓, cycE/CCNE↓, cycD1/CCND1↓, CDK2↓, CDK6↓, CDK4↓, YAP/TEAD↓, TFE3↑, mTORC1↓, mitResp↓, OCR↓, compI↓, MMP↓, ROS↑, SOD2↑, ATP↓, eff↓, mitA↓, P-gp/ABCB1↓, TumVol↓,

8028-

IVM,

Ivermectin as an Alternative Anticancer Agent: A Review of Its Chemical Properties and Therapeutic Potential

Review,

Var,

*BioAv↝, Apoptosis↑, TumCP↓, Wnt↓, β-catenin/ZEB1↓, TumCG↓, TumMeta↓, PI3K↓, Akt↓, mTOR↓, TumPF↓, CSCs↓, eff↑, ChemoSen↑, mtDam↑, MMP↓, ATP↓, ROS↑, NF-kB↓, BAX↑, Casp3↑, Casp9↑, ICD↑, Ki-67↓, PSA↓, YAP/TEAD↓,

8029-

IVM,

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

Review,

Var,

TumCP↓, Apoptosis↑, Wnt↓, β-catenin/ZEB1↓, Akt↓, mTOR↓, BBB∅, ROS↑, MMP↓, Casp3↓, Casp9↑, TumCCA↑, P53↑, cMyc↓, MMP9↓, HSP27↓, ICD↑, eff↑, *AntiP↑,

Showing Research Papers: 1 to 16 of 16

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

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiP↓, 1, AntiP↑, 6, Stroke↝, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1,

Functional Outcomes(tgid=23) ⓘ

AntiCan↓, 1, AntiDiabetic↑, 1, cardioP↑, 1, neuroP↑, 1, toxicity↓, 1, toxicity↑, 1,

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 2,
Total Targets: 12

Scientific Paper Hit Count for: ROS, Reactive Oxygen Species

16 Ivermectin
1 Photodynamic Therapy
1 doxorubicin

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#:10  Target#:275  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

Ivermectin / ROS Cancer Research Results

Ivermectin Mechanistic Profile

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) ⓘ

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) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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