itraconazole / PSA 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)
PSA, prostate-specific antigen: Click to Expand ⟱
Source:
Type:
Prostate-Specific Antigen (PSA) is a protein produced by both normal and malignant cells of the prostate gland. PSA testing is commonly used as a screening tool for prostate cancer.
Elevated levels of PSA in the blood can indicate the presence of prostate cancer, but they can also be caused by other conditions, such as benign prostatic hyperplasia (BPH) or prostatitis (inflammation of the prostate).

PSA is a clinical biomarker.
Scientific Papers found: Click to Expand⟱
2179- itraC,    Repurposing itraconazole for the treatment of cancer
- Review, Var, NA
HH↓, angioG↓, TumCCA↑, MDR1↓, P-gp↓, mTOR↓, VEGF↓, Smo↓, Gli1↓, OS↑, PSA↓,

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 Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Gli1↓, 1,   HH↓, 1,   mTOR↓, 1,   Smo↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

PSA↓, 1,  

Drug Metabolism & Resistance ⓘ

MDR1↓, 1,  

Clinical Biomarkers ⓘ

PSA↓, 1,  

Functional Outcomes ⓘ

OS↑, 1,  
Total Targets: 12

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PSA, prostate-specific antigen
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#:264  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

Home Page