Inoscavin A Cancer Research Results

InA, Inoscavin A: Click to Expand ⟱
Features:
Inoscavin A was obtained from Sanghuangporus vaninii by the classic phytochemical separation technology.

Inoscavin A — a naturally occurring polyphenolic pyrone and hispidin-derived fungal secondary metabolite with antioxidant and experimental anticancer activity. It is commonly abbreviated InA and has the molecular formula C25H18O9 and molecular weight approximately 462.4 g/mol. It has been isolated from medicinal fungi including Sanghuangporus vaninii, Sanghuangporus baumii (formerly Phellinus baumii), and Inonotus xeranticus. In cancer models, its best-supported molecular action is inhibition of Smoothened and downstream Hedgehog signaling. Inoscavin A remains an experimental natural product rather than an approved drug or established supplement-derived anticancer agent.

Primary mechanisms (ranked):

  1. ↓ Smoothened signaling, producing downstream ↓ Hedgehog pathway activity including reduced GLI1 signaling.
  2. ↑ apoptosis associated with mitochondrial membrane-potential disruption and suppression of tumor-cell survival.
  3. ↓ proliferation and clonogenic growth in colorectal cancer cells.
  4. ↓ tumor-cell migration and invasion.
  5. ↓ lipoxygenase activity, with an experimentally measured IC50 of approximately 6.8 µM; cancer relevance is secondary and not established as the principal anticancer mechanism.
  6. Free-radical scavenging and antioxidant activity; this is chemically well established but its contribution to anticancer activity is context-dependent and should not be assumed to mediate the observed tumor suppression.

Bioavailability / PK relevance: Human pharmacokinetics, oral bioavailability, metabolism, circulating concentrations, tissue penetration, and clinically tolerable exposure have not been established. Inoscavin A is therefore not presently amenable to evidence-based human dosing. Natural fungal abundance can also be low; one purification study recovered approximately 468 mg of purified Inoscavin A from 10 kg of S. vaninii sporocarp, emphasizing that mushroom intake cannot be equated with purified-compound exposure.

In-vitro vs systemic exposure relevance: The principal cancer evidence consists of HT-29 colorectal cancer cell experiments and an HT-29 xenograft mouse model. Because human plasma exposure data are unavailable, it cannot presently be determined whether experimentally active concentrations are achievable systemically in humans. The reported lipoxygenase IC50 of approximately 6.8 µM is an enzyme-assay concentration and should not be interpreted as an achievable therapeutic plasma concentration.

Clinical evidence status: Preclinical. Inoscavin A has demonstrated anticancer activity in cultured colorectal cancer cells and an HT-29 xenograft model, but there are no established human oncology trials, randomized clinical trials, approved indications, or validated adjunctive dosing protocols. The translational evidence is therefore substantially weaker than for clinically developed Smoothened inhibitors.

Inoscavin A Cancer-Relevant Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells Primary Effect Notes / Interpretation
1 Smoothened and Hedgehog signaling ↓ SMO; ↓ Hedgehog signaling; ↓ GLI1 Unknown ↓ proliferation; ↑ apoptosis Best-supported mechanistic axis. SMO overexpression partially rescued Inoscavin A-induced apoptosis, supporting SMO suppression as an upstream causal mechanism rather than merely an associated marker.
2 Apoptosis and mitochondrial integrity ↑ apoptosis; ↓ mitochondrial membrane potential Unknown ↑ programmed tumor-cell death Supported by mitochondrial membrane-potential and TUNEL assays in HT-29 models. The precise downstream mitochondrial death machinery has not been comprehensively established for purified Inoscavin A.
3 Cell proliferation and clonogenic survival ↓ proliferation; ↓ colony formation Unknown ↓ tumor growth Observed in HT-29 cells and supported by inhibition of tumor growth in an HT-29 xenograft model.
4 Migration and invasion ↓ migration; ↓ invasion Unknown ↓ aggressive tumor phenotype Supported by scratch-wound and transwell assays. Evidence is preclinical and largely limited to colorectal cancer models.
5 Lipoxygenase activity ↓ LOX (context-dependent) ↓ LOX (context-dependent) ↓ lipid-oxidation signaling Purified Inoscavin A inhibited lipoxygenase with an IC50 of approximately 6.8 µM. This is a direct biochemical activity, but its contribution to the demonstrated anticancer phenotype has not been established.
6 Free-radical scavenging ↓ oxidative radicals (context-dependent) ↓ oxidative radicals Antioxidant activity Inoscavin A was originally isolated as a potent fungal free-radical scavenger. Antioxidant activity should be regarded separately from its SMO-mediated anticancer mechanism because lowering ROS can theoretically be beneficial or detrimental depending on tumor context and therapy.
7 Clinical Translation Constraint Unknown human exposure Human safety poorly characterized Limits clinical interpretation No established human PK, bioavailability, therapeutic plasma concentration, maximum tolerated dose, cancer trial evidence, or approved therapeutic formulation. Current findings should therefore be classified as preclinical rather than clinically actionable.


Scientific Papers found: Click to Expand⟱
33- InA,    Inoscavin A, a pyrone compound isolated from a Sanghuangporus vaninii extract, inhibits colon cancer cell growth and induces cell apoptosis via the hedgehog signaling pathway
- vitro+vivo, Colon, NA
HH↓, Smo↓, TumCP↓, Apoptosis↑,
7613- InA,    Lipoxygenase Inhibitory Activity of Korean Indigenous Mushroom Extracts and Isolation of an Active Compound from Phellinus baumii
- Study, Nor, NA
*5LO↓,
7614- InA,    Inoscavin A, a new free radical scavenger from the mushroom Inonotus xeranticus
- Study, Nor, NA
*ROS↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,  

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

HH↓, 1,   Smo↓, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  
Total Targets: 4

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,  
Total Targets: 2

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#:100  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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