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High purity ginsenoside CK Compound K raw material for stroke support

High purity ginsenoside CK Compound K raw material for stroke support

  • High purity ginsenoside CK Compound K raw material for stroke support
High purity ginsenoside CK Compound K raw material for stroke support
Product Details:
Place of Origin: China
Brand Name: NUGLY
Certification: FDA,ISO9001,ISO22000,FSSC22000
Model Number: NUGLY CK
Payment & Shipping Terms:
Minimum Order Quantity: 100g
Price: FOB Shanghai USD150/100g
Packaging Details: 100g/bag
Delivery Time: 10-20 work days
Payment Terms: T/T,PAYPAL
Supply Ability: 1ton/year
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Detailed Product Description
Product: High Purity Ginsenoside CK Compound K Raw Material For Stroke Support Functions: Anti Cerebral Infarction And Prevention Of Stroke
Usage Method: Raw Materials For Health Food Suitable People: Raw Materials For Health Food
Color: White Grade: Food Grade
Storage: Dry And Shade Water Solubility: Water Soluble
Shelf Life: 24 Months CAS No.: 39262-14-1
Specification: Purity More Than 90% Molecular Weight: 622.873
Source: Ginseng Extract, Total Saponins Of Ginseng Molecular Formula: C36H62O8
Density: 1.05-1.1

1. Product Overview 

Ginsenoside Compound K (CK)
 
CAS: 39262-14-1
 
Also named: 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol, IH901, M1
 
Compound K is a rare deglycosylated protopanaxadiol-type ginsenoside. It is not naturally abundant in raw ginseng, mainly generated via enzymatic bioconversion from ginsenoside Rb1, Rb2 and Rc.
 

Compared with parent ginsenosides, CK features low molecular weight, high lipophilicity, superior oral bioavailability and blood-brain barrier penetration. Massive preclinical researches verify its potent neuroprotective effects against cerebral ischemia-reperfusion injury, making it a premium raw material for brain-health functional formulas targeting post-ischemic brain support.


 

2. Physicochemical Properties Section

Ginsenoside CK Physicochemical Profile

  • Chemical Formula: (boldsymbol{C_{36}H_{62}O_8})
  • Molecular Weight: 622.88 g/mol
  • CAS No.: 39262-14-1
  • Appearance: White to off-white crystalline powder
  • Melting Point: 181–183 °C
  • Lipophilicity (LogP): 5.50
  • Solubility: Soluble in methanol, ethanol, DMSO; slightly soluble in water
  • Stability: Hygroscopic; sealed, cool and dry storage required, avoid strong light
  • Production Technology: Enzymatic hydrolysis / microbial biotransformation
  • Available Specifications: HPLC 98%, 95%, 80%
Key Advantage for Brain Application
 

Low molecular weight & moderate lipophilicity enable CK to penetrate the blood-brain barrier (BBB) efficiently, directly acting on neurons and glial cells in brain tissue; most large-molecule original ginsenosides cannot cross BBB easily.


 

3. Mechanism Analysis: Neuroprotective Effects Against Cerebral Ischemic Injury

 
Ischemic stroke (cerebral infarction) triggers a cascade of damage: blood flow interruption → oxidative stress, microglia overactivation, mitochondrial dysfunction, neuronal apoptosis, inflammatory burst, and reperfusion secondary injury.
 
Preclinical MCAO/R (middle cerebral artery occlusion-reperfusion) animal models & OGD/R cell models demonstrate multiple protective pathways of Ginsenoside CK:

3.1 Stabilize Mitochondrial Dynamics & Energy Metabolism (Core Pathway)

Cerebral ischemia breaks mitochondrial fusion-fission balance, causing energy depletion and neuron death.
 
CK inhibits Mul1-mediated ubiquitination & degradation of Mfn2, elevates Mfn2 expression, suppresses DRP1 mitochondrial translocation. It restores mitochondrial fusion, reduces excessive mitochondrial fragmentation, maintains ATP synthesis, and alleviates bioenergy collapse in ischemic neurons.

3.2 Inhibit Neuronal Apoptosis & Programmed Cell Death

  • Upregulate anti-apoptotic protein Bcl-2, downregulate pro-apoptotic Bax; improve Bcl-2/Bax ratio
  • Suppress PTP1B activity, restore IRS1 signaling to block ischemia-triggered neuronal apoptosis
  • Inhibit PANoptosis (mixed inflammatory cell death) in ischemia-reperfusion tissue

3.3 Anti-Inflammation & Anti-Oxidative Stress

  • Restrain overactivation of microglia in ischemic penumbra
  • Downregulate NF-κB pathway, reduce release of TNF-α, IL-1β inflammatory cytokines
  • Activate Nrf2/ARE antioxidant pathway, eliminate excess ROS, reduce oxidative damage to nerve cells

3.4 Protect Blood-Brain Barrier Integrity

Reduce cerebral edema after ischemia, inhibit degradation of tight junction proteins; relieve BBB leakage caused by reperfusion injury, prevent further infiltration of inflammatory factors into brain parenchyma.

3.5 Improve Neurological Functional Recovery

Reduce the loss of Nissl bodies in neurons of ischemic areas, support survival of nerve cells in the penumbra region; create favorable conditions for post-ischemia neurological function repair.
Mechanism Summary Sentence (can be extracted for page subtitle):
 

Ginsenoside CK exerts multi-target neuroprotection against cerebral ischemia injury via regulating mitochondrial homeostasis, anti-apoptosis, anti-neuroinflammation and antioxidant activity.


 

4. Research In Vivo Data

All data derived from published MCAO/R rat cerebral ischemia-reperfusion models, suitable for quotation with clients; units & statistics retained, no exaggerated claims.
  1. Cerebral Infarct Volume (Dose-dependent efficacy)
     
    After MCAO/R operation, rats treated with Ginsenoside CK showed significantly reduced infarct volume:
  • Model group: 24.20% ±1.22%
  • CK 10 mg/kg group: 14.60% ±1.25%
  • CK 50 mg/kg group: 9.13% ±0.59%
     
    CK reduces infarct volume in a dose-dependent manner (p < 0.001).
  1. Neurological Score Improvement
     
    CK administration significantly lowered neurological deficit scores in ischemic rats, indicating alleviated motor and nerve dysfunction caused by focal cerebral ischemia.
  2. Neuronal Morphology Observation (Nissl Staining)
     
    Ischemia group presented massive neuron shrinkage, vacuolation and Nissl body loss.
     
    CK treatment group maintained intact neuronal morphology and obviously higher surviving neuron quantity in ischemic penumbra.
  3. Mitochondrial Morphology Observation (TEM)
     
    I/R group: severe mitochondrial swelling, cristae rupture, fragmentation.
     
    CK pretreatment: mitochondrial structure tended to be normal, reduced mitochondrial damage.
  4. Anti-inflammatory Index
     
    CK effectively suppressed the activation of microglia in cerebral ischemic cortex and decreased levels of pro-inflammatory cytokines in brain homogenate.
Disclaimer for data section:
 

All above results are obtained from preclinical cell & animal studies. Not clinical human trial data. Ginsenoside CK is developed as natural functional raw material.


 

5. Application Fields

  1. Functional raw materials for brain health dietary supplements
  2. Formula development for supporting post-ischemic neurological recovery
  3. Nootropic & cerebrovascular support health products
  4. Scientific research reagents for neuroscience & cerebral ischemia pharmacology
  5. Liposomal, nanocarrier brain-targeted formulation raw materials

  6.  

6. Product Advantages 

  1. High BBB permeability, direct action on central nervous system
  2. Multi-target neuroprotective mechanism for cerebral ischemic cascade injury
  3. Produced via controllable enzymatic conversion, stable purity, low impurity
  4. Rich published research data on cerebral ischemia models, easy for your product literature development
  5. Low acute toxicity, good safety profile for long-term oral formula
  6. Customizable purity & bulk packing; COA, HPLC, MS documents supplie

  7.  

 

LVEF↑37.9%

 

 

CK-MB ↓58.8%

 

Cerebral infarction area

↓37.4%

 

Troponin I

↓62.1%

 

 

Recommended dosage: CK 50-200mg/d

 

 

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