Database Query Results : Atorvastatin, ,

ATV, Atorvastatin: Click to Expand ⟱

Features: Statin

Atorvastatin is a statin, i.e., an inhibitor of HMG-CoA reductase, the rate-limiting enzyme of the mevalonate pathway. Clinically it is prescribed to lower LDL cholesterol and cardiovascular risk.

Atorvastatin — a synthetic small-molecule statin that competitively inhibits HMG-CoA reductase (HMGCR), the rate-limiting enzyme of the mevalonate (MVA) pathway. It is a clinically approved oral lipid-lowering drug (LDL-C reduction; ASCVD risk reduction) with extensive hepatic first-pass handling and pleiotropic vascular/anti-inflammatory effects. Classification: small-molecule drug; HMG-CoA reductase inhibitor (statin). Standard abbreviation(s): ATV; (brand: Lipitor). In oncology research, its main leverage is MVA-pathway suppression leading to reduced isoprenoid supply (FPP/GGPP) and impaired prenylation-dependent signaling (Ras/Rho family), with context-dependent chemosensitization/radiosensitization reported in preclinical and limited clinical settings.

Primary mechanisms (ranked):

HMGCR inhibition → ↓ mevalonate flux → ↓ FPP/GGPP isoprenoids → impaired protein prenylation (Ras/Rho/Rac signaling dependence)
↓ prenylation/↓ lipid-raft cholesterol support → attenuation of growth, survival, EMT/migration programs (context-dependent)
Compensatory sterol-feedback rewiring (SREBP2-driven upregulation of MVA genes; “restore-the-pathway” resistance axis)
Immuno-inflammatory modulation (often ↓ NF-κB–linked cytokine programs; tumor-context dependent)
Cell-stress outputs (apoptosis/autophagy modulation; mitochondrial stress/ROS changes in some models)
Therapy interaction phenotypes (chemosensitization and radiosensitization in selected contexts; not universal)

Bioavailability / PK relevance: Oral dosing with high hepatic extraction; exposure is strongly interaction-sensitive because atorvastatin is a CYP3A4 substrate and also uses hepatic transport (e.g., OATP1B1/1B3). Clinically meaningful systemic levels are achievable, but many anticancer in-vitro concentrations may exceed typical free plasma exposures; tumor delivery and intracellular “on-pathway” inhibition are therefore context- and dosing-dependent.

In-vitro vs systemic exposure relevance: Antiproliferative/EMT and apoptosis effects in cell culture are frequently reported at micromolar concentrations, which may be higher than unbound systemic exposures in humans; the most translatable mechanism is on-target MVA suppression with downstream prenylation stress, especially where tumors are MVA-addicted or combined with agents that block feedback/compensation.

Clinical evidence status: Approved drug for dyslipidemia/ASCVD prevention. In cancer: extensive preclinical literature plus observational associations; limited interventional oncology studies exist (including biomarker-focused trials and combination/adjunct concepts). Overall status: repurposing candidate with context-dependent signals; not an established anticancer therapy.

Across preclinical and observational contexts, atorvastatin tends to:
-DOWNREGULATE proliferative and survival signaling (via impaired prenylation)
-REDUCE inflammatory signaling (NF-κB–linked effects)
-MODULATE immune and stromal interactions
-SENSITIZE some tumors to chemotherapy or radiation (context-dependent)

-Epidemiologic studies suggest statin use is associated with reduced incidence or improved outcomes in some cancers (e.g., colorectal, prostate, breast).

Atorvastatin — cancer-relevant mechanistic axes (ranked)

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	Mevalonate pathway suppression	HMGCR ↓ → MVA flux ↓	HMGCR ↓ (hepatic target)	P/R	Depletes sterols + isoprenoids upstream	On-target mechanism; anticancer relevance rises in MVA-addicted tumors and when combined with strategies that prevent compensation.
2	Protein prenylation stress	Ras/Rho/Rac prenylation ↓ → signaling output ↓	Variable; typically tolerated at clinical doses	R	Disrupts membrane localization of key GTPases	Central downstream effector of anticancer activity; impacts proliferation, migration, cytoskeletal dynamics, and survival programs.
3	SREBP2 feedback and “restore-the-pathway” resistance	SREBP2 ↑ (often) → HMGCR/MVA genes ↑ (adaptive)	SREBP2 ↑ (homeostatic lipid control)	G	Adaptive rewiring that can blunt efficacy	Common translational constraint: tumors may upregulate MVA pathway, increase uptake, or rewire metabolism to bypass blockade.
4	Growth and survival signaling	PI3K–AKT ↔/↓, MAPK ↔/↓ (model-dependent)	Endothelial survival ↔/↑ (context-dependent)	R/G	Downshifts pro-survival signaling tone	Often secondary to prenylation/lipid-raft disruption; direction depends on oncogenic wiring and dose.
5	Migration, invasion, EMT	EMT ↓, motility ↓ (often)	Wound/repair migration ↔	G	Anti-migratory / anti-invasive phenotype	Mechanistically linked to Rho-family prenylation and cytoskeletal/ECM programs; may be clinically relevant in select settings.
6	Inflammation and NF-κB-linked cytokine programs	IL-6/IL-8/TNF-α ↓ (often)	Vascular inflammation ↓	R/G	Anti-inflammatory immunometabolic shift	Pleiotropic statin effects; may affect tumor microenvironment and therapy tolerance, but tumor-immune direction can be context-dependent.
7	ROS and mitochondrial stress	ROS ↑ (sometimes; dose-dependent)	Oxidative injury ↔/↓ in vascular contexts	P/R	Stress signaling that can promote apoptosis or sensitize to therapy	Reported in subsets of models; not universally primary. Separate “cancer cell ROS ↑” from “vascular protective” pleiotropy.
8	Cell death programs	Apoptosis ↑; autophagy ↔/↑ (model-dependent)	Generally cytoprotective at therapeutic dosing	R/G	Stress-induced cell fate shift	Often downstream of prenylation deficit + metabolic stress; strong effects often require higher concentrations or combinations.
9	Drug transport and resistance	P-gp ↓ (reported); efflux ↔/↓ (context-dependent)	Transporter effects ↔	R/G	Potential bioenhancement / chemosensitization	May contribute to combination effects, but clinical relevance is uncertain and interaction risk must be managed.
10	Radiosensitization and chemosensitization	RadioS ↑; ChemoSen ↑ (subset)	Normal tissue injury ↔/↓ (some contexts)	G	Adjunct therapy leverage (context-dependent)	Signals exist in preclinical and limited clinical/biomarker work; not a class-wide guarantee and may depend on tumor MVA reliance.
11	Clinical Translation Constraint	Free exposure may be below many in-vitro “kill” concentrations; adaptive SREBP2 feedback; tumor heterogeneity	Myopathy/rhabdomyolysis risk ↑ with interacting drugs; hepatic enzyme elevations; pregnancy contraindication	—	Defines practical therapeutic window	Major constraints: CYP3A4/transport interactions (e.g., strong inhibitors; grapefruit), muscle toxicity risk, and uncertain tumor delivery/on-target engagement at tolerated doses.

TSF legend: P: 0–30 min R: 30 min–3 hr G: >3 hr

Scientific Papers found: Click to Expand⟱

4988-

ATV,

Dipy,

Repurposing of the Cardiovascular Drug Statin for the Treatment of Cancers: Efficacy of Statin–Dipyridamole Combination Treatment in Melanoma Cell Lines

in-vivo,

Melanoma,

canine, human

HMGCR↓, Metastatic melanoma has a very poor prognosis. Statins, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR) inhibitors, are cholesterol-lowering agents with a potential for cancer treatment.
SREBP2↑, The inhibition of HMGCR by statins, however, induces feedback, which paradoxically upregulates HMGCR expression via sterol regulatory element-binding protein-2 (SREBP2)
SREBP2↓, Dipyridamole, an antiplatelet agent, is known to inhibit SREBP2 upregulation.
AntiAg↑,

5454-

ATV,

Interplay of mevalonate and Hippo pathways regulates RHAMM transcription via YAP to modulate breast cancer cell motility

Review,

BC,

HMG-CoA↓, Statins, inhibitors of mevalonate metabolic pathway
HMGCR↓, Statins are specific inhibitors of the 3-hydroxy-methylglutaryl CoA reductase (HMGCR)
TumCP↓, statins have recently been found to also have multiple anticancer effects such as antiproliferative, proapoptotic, antiinvasive, and radiosensitizing properties
RadioS↑,
CD44↓, n breast cancer, statins prevented metastasis by inhibiting CD44 expression through promoting p53 expression (25)
P53↑,

5453-

ATV,

Epidemiologic Analysis Along the Mevalonate Pathway Reveals Improved Cancer Survival in Patients Who Receive Statins Alone and in Combination With Bisphosphonates

Trial,

Var,

312,907 identified patients with cancer,

OS↑, Statin use before diagnosis was associated with improved overall survival compared with no treatment (hazard ratio [HR], 0.85; 95% CI, 0.80 to 0.91) and specifically in patients with leukemia, lung, or renal cancers.
eff↑, This study suggests that the combination of statins with drugs that affect isoprenylation, such as bisphosphonates, improves survival in patients with cancer.
other↝, However, patients younger than age 65 years in the comparison of statin users versus nonusers had improved survival, whereas those older than age 65 years did not.

5452-

ATV,

Mevalonate pathway in pancreatic ductal adenocarcinoma: mechanisms driving metabolic and cellular plasticity

Review,

Var,

ChemoSen↑, The study further highlighted that statins, which inhibit the mevalonate pathway, could significantly reduce protein glycosylation and enhance chemotherapy sensitivity by suppressing EMT signatures in PDAC organoid models.
HMG-CoA↓,
EMT↓,
Ferroptosis↑, cancer cells upregulate the mevalonate pathway to manage oxidative stress and evade ferroptosis and that inhibiting this pathway, either by statins or fatostatin, an SREBP1 inhibitor, can trigger ferroptotic death.
Hif1a↓, pharmacological inhibition of the mevalonate pathway using statins reduces HIF-1α levels

5451-

ATV,

In vitro and in vivo anticancer effects of mevalonate pathway modulation on human cancer cells

in-vitro,

BC,

MDA-MB-231

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

A172

TumAuto↑, cerivastatin, pitavastatin, and fluvastatin were the most potent anti-proliferative, autophagy inducing agents in human cancer cells including stem cell-like primary glioblastoma cell lines.
CSCs↓,
HMG-CoA↓, These data demonstrate that statins main effect is via targeting the mevalonate synthesis pathway in tumour cells.
TumCP↓, Statins inhibit proliferation/viability of human tumour cell lines
tumCV↓,
TumCCA↑, Statins induce cell cycle arrest in tumour cells
TumCG↓, Statins inhibit tumour growth in animal models
HMGCR↓, Statins are competitive inhibitors of HMGCR, which converts HMG-CoA to mevalonate.

5450-

ATV,

The Mevalonate Pathway in the Radiation Response of Cancer

vitro+vivo,

Var,

eff↑, Targeting the MVA pathway with statins and other inhibitors has shown promise in preclinical studies; however, clinical outcomes remain controversial, raising concerns about translating these findings into effective treatments.
RadioS↑, The Mevalonate Pathway in the Radiation Response of Cancer

5449-

ATV,

Pleiotropic effects of statins: A focus on cancer

NA,

Var,

lipid-P↓, Statins exhibit “pleiotropic” properties that are independent of their lipid-lowering effects.
TumCG↓, preclinical evidence suggests that statins inhibit tumor growth and induce apoptosis in specific cancer cell types.
Apoptosis↑,
ChemoSen↑, statins show chemo-sensitizing effects by impairing Ras family GTPase signaling.
RAS↓,
HMG-CoA↓, Statins are potent, competitive inhibitors of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase (HMGCR).
HMGCR↓,
LDL↓, Statins reduce blood plasma cholesterol levels by decreasing de novo cholesterol biosynthesis and by inducing changes in low density lipoprotein (LDL) receptor expression [2].
toxicity↓, Due to the well-established safety profile of statins, such studies are less expensive than the development of novel drugs.
Risk↓, statin use in cancer patients was associated with reduced cancer-related mortality. The risk of cancer death was significantly lower in postmenopausal women
P21↑, Other proposed mechanisms leading to an increase of p21 levels include the release of promoter-associated histone deacetylase and inhibition of histone deacetylase
HDAC↓,
Bcl-2↓, Statins trigger the intrinsic apoptosis pathway and decrease Bcl-2 protein expression [[154], [155], [156]], increase Bax and BIM protein expression [[156], [157], [158], [159]], and activate several caspases
BAX↑,
BIM↑,
Casp↑,
cl‑PARP↑, thereby increasing cleaved PARP-1 levels.
MMP↓, different tumor cell lines (breast, brain, and lung) showed that simvastatin-induced apoptosis is dependent on decreasing mitochondrial membrane potential and increasing reactive oxygen species (ROS) production
ROS↑,
angioG↓, Statins inhibit angiogenesis and metastasis
TumMeta↓,
PTEN↑, n breast cancer xenografts, simvastatin prevented tumor growth by reducing Akt phosphorylation and BclXL transcription, while simultaneously increasing the transcription of pro-apoptotic/anti-proliferative PTEN
eff↑, In mice, the administration of a combination of celecoxib and atorvastatin was more effective than each individual treatment, and effectively prevented prostate cancer progression from androgen dependent to androgen independent
OS↑, Long-term statin use may improve survival in GBM patients treated with temozolomide chemotherapy
Remission↑, statin use during or after chemotherapy is not associated with improved disease-free-, recurrence-free-, or overall survival in stage II colon cancer patients

5448-

ATV,

Beyond cardiovascular health: The pharmacotherapeutic potential of statins in oncology

Review,

Var,

Apoptosis↑, Despite statins’ ability to induce apoptosis or autophagy, arrest cell cycle, or modulate favorable epigenetic reprogramming, their efficacy is highly context-dependent
TumAuto↑,
TumCCA↑,
BioAv↓, Challenges such as statin resistance, low bioavailability and pharmacokinetic variability further complicate their application in oncology.
eff↑, including nanoparticle-based drug delivery systems and combination therapies with chemotherapy, radiotherapy or immunotherapy, appear to help overcome these limitations.
HMGCR↓, statins reduce cholesterol levels by targeting HMGCR
LDL↓,
cardioP↑, statins have become a cornerstone in the management of hypercholesterolemia and the prevention of cardiovascular diseases [23], [24], [25], [26].
AntiTum↑, Notably, while research suggests that statins possess anti-tumor effects, evidence remains conflicting and highly context-dependent
ChemoSen↑, suggest that statins can sensitize cancer cells to chemotherapy and radiotherapy, potentially improving treatment outcomes,
RadioS↑,
toxicity↓, Statins are widely regarded as safe and well-tolerated. However, like any medication, they are not without potential side effects, though these are generally mild [232].

5447-

ATV,

The Mevalonate Pathway, a Metabolic Target in Cancer Therapy

Review,

Var,

Risk↓, increasing amount of data, from preclinical and epidemiological studies, that support an inverse association between the use of statins, potent inhibitors of MVA biosynthetic pathway, and mortality rate in specific cancers
Dose↑, cancer treatment demands the use of relatively high doses of single statins for a prolonged period, thereby limiting this therapeutic strategy due to adverse effects.
ChemoSen↑, synergistic effects of tolerable doses of statins with conventional chemotherapy might enhance efficacy with lower doses of each drug and, probably, reduce adverse effects and resistance.
chemoP↑,
HMG-CoA↓, potential use of MVA pathway inhibitors to improve therapeutic window in cancer.
EMT↓, statins may suppress epithelial-mesenchymal transition (EMT) program together with the inhibition of cancer stem cell generation, maintenance, and expansion
CSCs↓,
HH↝, inhibitors of MVA pathway (e.g., statins) that modulate Hh pathway activity could represent potential drugs in Hh pathway-related cancers.
YAP/TEAD↝, MVA participates in the regulation of YAP-TAZ expression and transcriptional activity and reveal an original process through which statins have anticancer effects.

5446-

ATV,

Targeting the Mevalonate Pathway in Cancer

Review,

Var,

EMT↓, In a phase II clinical trial of atorvastatin in breast cancer, RhoB, a tumor suppressing Rho family member, was increased and promoted the reversion of EMT, demonstrating that EMT can be targeted in the clinic [47,48].
HMG-CoA↓, first and foremost class of mevalonate pathway inhibitors: statins [4].

5445-

ATV,

Atorvastatin

NA,

Nor,

*cardioP↑, atorvastatin is FDA-approved for the prevention of cardiovascular events in patients with cardiac risk factors and abnormal lipid profiles.[1]
*LDL↓, patients should be prescribed high-intensity statin therapy to achieve a ≥50% reduction in low-density lipoprotein cholesterol (LDL-C) and reduce the risk of major adverse cardiovascular events (MACE).
HMG-CoA↓, Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.[12]
Half-Life↝, Atorvastatin is rapidly absorbed after oral administration with a peak plasma concentration at 1 to 2 hours. The half-life of atorvastatin is about 14 hours, while its active metabolites have a half-life of about 20 to 30 hours.
BioAv↓, The bioavailability is low at 14% due to extensive first-pass metabolism.
Dose↝, Atorvastatin is available as atorvastatin calcium tablets in strengths of 10, 20, 40, and 80 mg. It is also available as an oral suspension in a strength of 20 mg/5 mL.[20]

4986-

ATV,

Dipy,

The combination of statins and dipyridamole is effective preclinically in AML, MM, and breast cancer

Review,

Var,

HMG-CoA↓, Statins are drugs that have been utilized for years to treat hyperlipidemia through inhibition of the rate-limiting enzyme of the mevalonate (MVA) pathway, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)
AntiAg↑, Dipyridamole (DP), a commonly prescribed anti-platelet agent potentiated the anti-cancer effects of atorvastatin
eff↑, DP-statin combination was synergistic and capable of inducing apoptosis in a variety of acute myelogenous leukemia (AML), MM and breast cancer cell lines.
Apoptosis↑, DP-statin combination also induced apoptosis in primary AML patient samples, but was not toxic to normal PBSCs.
selectivity↑,
*toxicity↓,
TumCG↓, In an in vivo AML tumor model, the DP-statin combination was found to be effective at inhibiting tumor growth.
PDE4↓, DP is known to elicit numerous effects, amongst them, phosphodiesterase (PDE) inhibition
other↑, . As both statins and DP are pre-approved for use in humans, off-patent, and readily available, they have the potential to directly impact patient care.

4985-

ATV,

Dipy,

Repurposing of the Cardiovascular Drug Statin for the Treatment of Cancers: Efficacy of Statin-Dipyridamole Combination Treatment in Melanoma Cell Lines

in-vivo,

Melanoma,

SK-MEL-28

in-vitro,

BC,

MDA-MB-435

HMG-CoA↓, inhibition of HMGCR by statins, however, induces feedback, which paradoxically upregulates HMGCR expression via sterol regulatory element-binding protein-2 (SREBP2)
SREBP2↓, Dipyridamole, an antiplatelet agent, is known to inhibit SREBP2 upregulation.
eff↑, the inexpensive and frequently prescribed statin–dipyridamole combination therapy may lead to new developments in the treatment of melanoma and may potentiate the effects of vemurafenib for the targeted therapy of BRAF V600E-mutation bearing melanoma
HMGCR⇅, Atorvastatin Upregulates HMGCR mRNA Expression in a Dose-Dependent Manner While Dipyridamole Tends to Downregulate It
ChemoSen↑, combining conventional chemo- and/or targeted therapies with new drugs to improve therapeutic outcomes

4982-

ATV,

Inhibiting the mevalonate pathway with atorvastatin alters gut microbiota and has potential as an anti-cancer treatment for ovarian cancer

in-vivo,

Ovarian,

Female C57BL/6 mice

HMG-CoA↓, Statins, a mevalonate (MVA) pathway antagonist, are widely used to treat and prevent hypercholesterolemia by blocking cellular production of cholesterol.
GutMicro↑, Furthermore, statins have been shown to induce significant changes in intestinal enterotypes in both humans and mice. statins favorably alter the intestinal microbiome

4981-

ATV,

Crosstalk between Statins and Cancer Prevention and Therapy: An Update

Apoptosis↑, The anti-tumor activity of statins is largely related to their ability to induce apoptosis by targeting cancer cells with high selectivity.
selectivity↑,
eff↑, Combining statins with histone deacetylase inhibitors can induce a synergistic anticancer effect.
HMG-CoA↓, 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, known as statins, are a commonly used and well-tolerated class of drugs used in lipid disorders,
*cardioP↑, Their effectiveness in preventing the development of cardiovascular diseases makes statins one of the most widely used drugs
OS↑, On the other hand, improved survival in patients with hepatocellular carcinoma, colon cancer or prostate cancer is visible after the use of any statin
IL1β↓, statins inhibit the synthesis of cytokines, including interleukin (IL-) IL-1β, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α)
IL6↓,
IL8↓,
TNF-α↓,
TumAuto↑, Simvastatin-induced autophagy has been reported in rhabdomyosarcoma cells [
Histones↝, Statins are also involved in the regulation of the histone acetylation level.
ac‑H3↑, Studies indicate that statins increase histone H3 and H4 acetylation as well as inhibit class I and II HDACs
ac‑H4↑,
HDAC↓,

4980-

ATV,

A review of effects of atorvastatin in cancer therapy

Review,

Var,

HMG-CoA↓, atorvastatin as a reductase (HMG-CoA) inhibitor might affect proliferation, migration, and survival of cancer cells.
TumCP↓,
TumCMig↓,

4979-

ATV,

Rad,

Short‐Term Statin Treatment Reduces, and Long‐Term Statin Treatment Abolishes, Chronic Vascular Injury by Radiation Therapy

in-vivo,

Nor,

C57Bl/6 mice were pretreated with pravastatin for 72 hours and then exposed to 12 Gy X‐ray head‐and‐neck irradiation

radioP↑, Treatment with pravastatin for 24 hours after irradiation reduced the loss of endothelium‐dependent vasorelaxation and protected against enhanced vasoconstriction.
radioP↑, Treatment with pravastatin for 1 year after irradiation completely reversed irradiation‐induced changes.

4978-

ATV,

Rad,

Atorvastatin Sensitizes Breast and Lung Cancer Cells to Ionizing Radiation

in-vitro,

BC,

A549

Apoptosis↑, ATV increased the percentage of apoptotic cells in irradiated breast and lung cancer cells.
RadioS↑, demonstrates that ATV has radiosensitizing effect on breast and lung cancer cells through increasing apoptosis, ROS production and cell death induced by IR.
TumCP↓, ATV exhibited anti-proliferative effect on cancer cells and increased cell death induced by IR.
ROS↑, ATV increased ROS production in irradiated cells.

4987-

Dipy,

ATV,

Enhanced cardioprotection against ischemia-reperfusion injury with a dipyridamole and low-dose atorvastatin combination

in-vivo,

Nor,

rats

*cardioP↑, In conclusion, low-dose ATV and DIP had synergistic effects in reducing myocardial IS and activation of Akt and eNOS.
*Akt↑,
*eNOS↑,

4984-

Dipy,

ATV,

Immediate Utility of Two Approved Agents to Target Both the Metabolic Mevalonate Pathway and Its Restorative Feedback Loop

in-vitro,

AML,

eff↑, The statin–dipyridamole combination was synergistic and induced apoptosis in multiple myeloma and AML cell lines and primary patient samples, whereas normal peripheral blood mononuclear cells were not affected.
Apoptosis↑,
selectivity↑,
TumCG↓, This novel combination also decreased tumor growth in vivo.
HMG-CoA↓, Statins block HMG-CoA reductase (HMGCR), the rate-limiting enzyme of the MVA pathway.
HMGCR↑, Dipyridamole blunted the feedback response, which upregulates HMGCR and HMG-CoA synthase 1 (HMGCS1) following statin treatment.

4983-

Dipy,

ATV,

Targeting tumor cell metabolism via the mevalonate pathway: Two hits are better than one

Review,

Var,

HMG-CoA↓, Statins are promising anticancer agents that target the mevalonate pathway
AntiTum↓, dipyridamole inhibits this feedback response and potentiates statin antitumor activity.
eff↑, this combination of 2 FDA-approved drugs has the potential to be fast-tracked to cancer patient care.

1802-

NarG,

ATV,

Bioenhancing effects of naringin on atorvastatin

in-vivo,

Nor,

AST along with naringin (15 and 30 mg/kg)

Rats

BioEnh↑, a natural bioenhancer and reported to enhance the bioavailability of drugs by inhibiting cytochrome P450 and P-glycoprotein (P-gp)
LDL↓, Animals received AST along with naringin (15 and 30 mg/kg) shown higher percent reduction in both cholesterol and triglycerides levels
P450↓,
P-gp↓,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 22

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Core Metabolism/Glycolysis ⓘ

LDL↓, 1,

Cell Death ⓘ

Akt↑, 1,

Angiogenesis & Vasculature ⓘ

eNOS↑, 1,

Functional Outcomes ⓘ

cardioP↑, 3, toxicity↓, 1,
Total Targets: 5

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

Database Query Results : Atorvastatin, ,

Atorvastatin — cancer-relevant mechanistic axes (ranked)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Angiogenesis & Vasculature ⓘ

Functional Outcomes ⓘ

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