itraconazole / TumCP Cancer Research Results

itraC, itraconazole: Click to Expand ⟱
Features:
Itraconazole is a medication used in the management and treatment of fungal infections.

Itraconazole (ITZ; brand Sporanox) — oral triazole antifungal (drug). Oncology relevance is mainly repurposing research (not an approved anticancer indication).

Primary mechanisms (conceptual rank):
1) ↓ Ergosterol synthesis via fungal CYP51 inhibition (primary approved antifungal MoA)
2) ↓ Hedgehog signaling (SMO pathway inhibition; anticancer repurposing)
3) ↓ Angiogenesis / endothelial signaling (anti-angiogenic effects reported; AKT/mTOR signaling suppression in endothelium models)
4) ↑ Autophagy / cell-cycle arrest (model-dependent anticancer phenotypes)

Bioavailability / PK relevance: Oral bioavailability ~55%; capsules absorb best with a full meal; reduced by low gastric acidity (PPIs/H2 blockers). Strong CYP3A4 inhibitor with major drug–drug interaction burden; boxed warning/avoid in ventricular dysfunction/CHF except for serious infections.

In-vitro vs oral exposure: Many anticancer in-vitro effects occur at concentrations that may exceed (or sit near the upper range of) achievable systemic exposure; clinical relevance is formulation/PK-limited and indication-specific.

Clinical evidence status: Approved antifungal; oncology evidence is preclinical + small human/phase II repurposing signals (no oncology RCT approval).


Cancer pathways:
-inhibit VEGF
-inhibit Hedghog Signaling Pathway
-P-glycoprotein Inhibition
-mTOR Pathway

Itraconazole — Cancer vs Normal Cell Pathway Map

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Hedgehog (SMO → GLI) ↓ (model-dependent) ↔ R/G Reduced HH-driven proliferation Repurposing core: inhibits SMO/HH signaling in HH-dependent tumors (e.g., BCC contexts); not an approved oncology indication.
2 Angiogenesis (endothelial growth signaling) ↓ vascular support ↓ endothelial proliferation (context-dependent) R/G Anti-angiogenic effect Identified in repurposing screens as anti-angiogenic; often framed via endothelial signaling suppression (AKT/mTOR in some models).
3 AKT / mTOR ↓ (model-dependent) ↓ (endothelium; context-dependent) R/G Reduced anabolic/survival signaling Reported in endothelial and some tumor models; often tied to growth inhibition and vascular effects.
4 Autophagy ↑ (model-dependent) ↔ / ↑ (stress-dependent) R/G Stress adaptation / growth arrest Often described as autophagic growth arrest; can be cytostatic or contribute to death depending on context.
5 Cell cycle ↓ proliferation ↔ G Checkpoint arrest Phenotype reported across models; typically requires sustained exposure.
6 Apoptosis (intrinsic; caspases) ↑ (model-dependent) ↔ / ↑ (high exposure) R/G Programmed cell death Usually secondary to pathway inhibition / metabolic stress; varies by tumor type and exposure.
7 ROS ↔ (not primary) ↔ P/R No dominant redox program ROS is not a canonical primary ITZ mechanism versus HH/angiogenesis; include only with model-specific evidence.
8 NRF2 ↔ ↔ R/G No primary modulation No consistent NRF2-first mechanism at therapeutic exposure in the repurposing literature.
9 Ferroptosis ↔ (insufficiently established) ↔ R/G Not a canonical ITZ axis Not a standard mechanistic claim for ITZ; treat as investigational unless a specific study supports it.
10 HIF-1α ↓ (indirect; context-dependent) ↔ G Hypoxia/angiogenesis coupling reduction Primarily indirect via anti-angiogenic effects; tumor hypoxia biology can be complex.
11 Ca²⁺ signaling ↔ ↔ P/R No primary role Not a recognized primary ITZ axis.
12 Clinical Translation Constraint ↓ (constraint) ↓ (constraint) — DDIs + exposure variability Major constraints: CYP3A4 inhibition (drug–drug interactions), absorption dependence on meal/acidity, CHF/ventricular dysfunction warning, and repurposing effects that may require higher exposure or specific tumor dependence (HH).

TSF legend: P: 0–30 min (direct target engagement); R: 30 min–3 hr (acute signaling shifts); G: >3 hr (gene-regulatory/phenotype outcomes)
TumCP, Tumor Cell proliferation: Click to Expand ⟱
Source:
Type:
Tumor cell proliferation is a key characteristic of cancer. It refers to the rapid and uncontrolled growth of cells that can lead to the formation of tumors.
Scientific Papers found: Click to Expand⟱
2180- itraC,    Repurposing Drugs in Oncology (ReDO)—itraconazole as an anti-cancer agent
- Review, Var, NA
Dose↝, toxicity↝, BioAv↑, Half-Life↝, BioAv↑, Dose↝, HH↓, TumAuto↑, Akt↓, mTOR↓, angioG↓, MDR1↓, TumCP↓, eff↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

Akt↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HH↓, 1,   mTOR↓, 1,  

Migration ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   Dose↝, 2,   eff↑, 1,   Half-Life↝, 1,   MDR1↓, 1,  

Functional Outcomes ⓘ

toxicity↝, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: TumCP, Tumor Cell proliferation
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#:312  Target#:327  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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