Cynanbungeigenin C (CBC) and D (CBD) / AST Cancer Research Results

CBC/D, Cynanbungeigenin C (CBC) and D (CBD): Click to Expand ⟱
Features:

Cynanbungeigenin C and D — Cynanbungeigenin C (CBC) and Cynanbungeigenin D (CBD) are a pair of epimeric C21 steroidal natural products isolated from Cynanchum bungei Decne. They are best classified as plant-derived small-molecule Hedgehog pathway inhibitors, with reported activity at or near the GLI transcriptional effector level rather than as canonical Smoothened-only inhibitors. The abbreviation CBC/D is preferable in this database entry because CBC and CBD also commonly refer to cannabinoids.

Primary mechanisms (ranked):

  1. Hedgehog pathway suppression through GLI-level blockade, reducing downstream GLI1-dependent transcriptional output.
  2. Suppression of Hedgehog-dependent medulloblastoma growth and tumor-propagating signaling.
  3. Anti-proliferative and pro-apoptotic tumor effects, strongest evidence currently from medulloblastoma models for CBC/D and colorectal cancer models for the CBC derivative CBC-1.
  4. Drug-development constraint: poor aqueous solubility of parent CBC, motivating CBC-1 derivative synthesis with improved solubility and stronger colorectal cancer activity.

Bioavailability / PK relevance: Human pharmacokinetics, oral bioavailability, metabolism, and clinically achievable exposure are not established. Parent CBC has reported poor water solubility; CBC-1 was developed partly to improve this limitation. Mouse in-vivo activity is preclinical and should not be treated as evidence of human exposure feasibility.

In-vitro vs systemic exposure relevance: The mechanistic evidence is concentration-driven and mostly preclinical. Because human PK data are absent, common in-vitro concentrations cannot yet be judged against achievable systemic exposure. Solubility and formulation are central translation constraints.

Clinical evidence status: Preclinical only. Evidence consists mainly of natural-product isolation, cell-based Hedgehog/GLI assays, medulloblastoma tumor models, and a newer CBC-derived GLI1 inhibitor study in colorectal cancer. No human oncology trials or regulatory approval were identified for CBC/D or CBC-1.

CBC/D Cancer Mechanism Matrix

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 GLI transcriptional output ↓ GLI signaling Not established G Blocks Hedgehog signaling at the GLI level Core mechanism for CBC/D in Hedgehog-dependent medulloblastoma; CBC-1 derivative evidence supports direct GLI1 targeting in CRC models.
2 Hedgehog pathway ↓ HH pathway activity Not established G Suppresses oncogenic HH pathway dependence Most relevant where tumors depend on SHH/HH-GLI signaling; likely context-dependent across cancers.
3 Medulloblastoma growth ↓ proliferation and tumor growth Not established G Antitumor activity in HH-dependent medulloblastoma models Parent CBC/D evidence is strongest in this disease model rather than broad pan-cancer evidence.
4 Apoptosis ↑ apoptosis Not established G Cell death secondary to GLI1 suppression Best documented for CBC-1 derivative in colorectal cancer; parent CBC/D apoptosis evidence should be marked derivative-supported unless confirmed in the original paper.
5 Tumor progression ↓ tumor-propagating capacity Not established G Reduced malignant growth phenotype tumor cell proliferation or tumor progression suppression; external evidence supports growth suppression more clearly than migration-specific effects.
6 ROS NRF2 Ca²⁺ Glycolysis HIF-1α Not established Not established G No primary evidence found Do not force redox, NRF2, calcium, glycolysis, or hypoxia axes unless a direct CBC/D paper supports them.
7 Clinical Translation Constraint Solubility-limited parent compound Safety window not established G PK and formulation uncertainty Parent CBC poor water solubility and absent human PK are the main database constraints; CBC-1 derivative improves solubility but remains preclinical.

TSF legend:

P: 0–30 min

R: 30 min–3 hr

G: >3 hr
AST, Aspartate Aminotransferase: Click to Expand ⟱
Source:
Type:
AST (Aspartate Aminotransferase) is an enzyme found in various tissues throughout the body, including the liver, heart, muscles, kidneys, and brain. Elevated levels of AST in the blood can be an indicator of tissue damage or disease.
AST levels can be elevated in certain types of cancer.
Used as a clinical biomarker for Liver function


Scientific Papers found: Click to Expand⟱
6254- CBC/D,    Cynanchum auriculatum Royle ex Wight., Cynanchum bungei Decne. and Cynanchum wilfordii (Maxim.) Hemsl.: Current Research and Prospects
- Review, Var, NA
*neuroP↑, *Imm↑, *Inflam↓, CSCs↓, HH↓, Gli↓, AST↓, ALAT↓, MDA↓, hepatoP↑, *NRF2↑, *HO-1↑, NF-kB?, GSK‐3β↓, β-catenin/ZEB1↓, COX2↓, MMP2↑, MMP9↓, BioAv↑,

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:


Redox & Oxidative Stress ⓘ

MDA↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   Gli↓, 1,   GSK‐3β↓, 1,   HH↓, 1,  

Migration ⓘ

MMP2↑, 1,   MMP9↓, 1,   β-catenin/ZEB1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB?, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NRF2↑, 1,  

Immune & Inflammatory Signaling ⓘ

Imm↑, 1,   Inflam↓, 1,  

Functional Outcomes ⓘ

neuroP↑, 1,  
Total Targets: 5

Scientific Paper Hit Count for: AST, Aspartate Aminotransferase
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#:67  Target#:691  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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