Food‑grade ginsenoside CK ingredient for body inflammation care

Ginsenoside Compound K (CK) — Inflammation Modulation & Immune Balance

Product Overview

Ginsenoside Compound K (CK) — CAS: 39262-14-1 — is a rare deglycosylated protopanaxadiol-type ginsenoside produced via enzymatic bioconversion from major ginsenosides Rb1, Rb2 and Rc.

Unlike parent ginsenosides, CK features low molecular weight, high oral bioavailability and efficient tissue distribution. Extensive preclinical research demonstrates its potent multi-target anti-inflammatory activity, modulating both acute and chronic inflammatory pathways through NF-κB, NLRP3 inflammasome and macrophage polarization regulation — making it a premium functional ingredient for immune-inflammatory balance formulas.

Compliance Note: CK is a natural dietary raw material. All claims are based on preclinical study data.

Physicochemical Properties

Anti-Inflammatory Mechanism
 

Chronic low-grade inflammation involves a cascade of immune dysregulation: pro-inflammatory cytokine overproduction, NF-κB hyperactivation, NLRP3 inflammasome assembly, and M1 macrophage polarization. Ginsenoside CK modulates these pathways at multiple levels:

1. Inhibit NF-κB Signaling Pathway

CK suppresses IκBα phosphorylation and degradation, blocking NF-κB nuclear translocation. This downregulates transcription of pro-inflammatory genes including TNF-α, IL-1β, IL-6 and iNOS, reducing systemic inflammatory response.

2. Suppress NLRP3 Inflammasome Activation

CK inhibits NLRP3 inflammasome assembly and caspase-1 activation, reducing mature IL-1β and IL-18 secretion — a key mechanism for alleviating chronic sterile inflammation and metabolic inflammation.

3. Regulate Macrophage Polarization

CK promotes macrophage shift from pro-inflammatory M1 phenotype toward anti-inflammatory M2 phenotype, rebalancing tissue immune microenvironment and supporting resolution of inflammation.

4. Mitigate MAPK / JNK Inflammatory Cascade

CK modulates MAPK family (p38, ERK, JNK) phosphorylation, attenuating downstream inflammatory mediator production and reducing oxidative stress-induced inflammatory amplification.

Research Data

All data derived from peer-reviewed preclinical studies (cell & animal models). Not clinical human trial data.

In Vitro Data

In Vivo Data

• Acute inflammation model (carrageenan-induced paw edema): CK 50 mg/kg significantly reduced paw edema by ~48% at 4h, comparable to reference anti-inflammatory agents.

• DSS-induced colitis model: CK treatment reduced disease activity index (DAI), preserved colon length, and downregulated colonic TNF-α and IL-6 levels.

• Neuroinflammation model (LPS-induced): CK crossed BBB and suppressed microglial activation, reducing brain IL-1β and TNF-α by ~40%.

• Adipose tissue inflammation (high-fat diet): CK reduced macrophage infiltration in adipose tissue and improved metabolic inflammatory profile.

Application Fields

Product Advantages

1. Multi-target mechanism — addresses NF-κB, NLRP3, macrophage and MAPK pathways simultaneously

2. High bioavailability — deglycosylated structure enables superior oral absorption and tissue distribution

3. BBB penetration — effective for neuroinflammation-related applications

4. Controllable enzymatic production — stable purity, low impurity profile, batch-to-batch consistency

5. Strong preclinical evidence — rich published data across multiple inflammation models

6. Good safety profile — low acute toxicity, suitable for long-term oral supplementation

Recommended dosage:
CK 50-150mg/d daily inflammation regulation