PCC1 Delivery Advances

Innovative PCC1 Delivery Technology

As a promising anti-aging candidate compound, Procyanidin C1 (PCC1) faces a significant challenge: its limited bioavailability. Addressing this issue is crucial, as it directly impacts the compound's full efficacy in vivo.

PCC1-Enriched Lecithin Phytosomal Formulation

Our PCC1-Enriched lecithin phytosomal formulation provides a solution. Utilizing advanced Phospholipid Complexation technology, our PCC1-formulation creates a stable phytosomal carrier system by combining high-purity procyanidin fraction PCC1 with lecithin. Through biomimetic membrane design, this innovative technology not only optimizes PCC1's stability, gastrointestinal tolerance, but also improve transmembrane transport efficiency at the molecular level.

Improvement in Stability

The phospholipid complex effectively encapsulates PCC1, which is rich in polyphenolic nucleophilic sites, thereby mitigating chain degradation caused by free radicals, metal ions, and light exposure. This encapsulation strategy minimizes molecular aggregation and precipitation, preserving an optimal dispersion state while establishing a "buffer zone" that delays degradation processes, enhancing the stability and bioavailability of PCC1.

The accelerated stability testing results showed that after 7 days at 40°C and 75% RH:

  • Unencapsulated PCC1 decreased to 76%
  • PCC1 encapsulated in egg yolk lecithin phytosomes retained 93%
  • Soybean lecithin group maintained 90%
  • Representing improvements in preservation efficiency of 17% and 14%, respectively

Under ambient conditions (20°C, RH < 30%), no significant changes were observed in the two PCC1 lecithin formulations over one month, while the unencapsulated PCC1 degraded by approximately 10%.

Experimental Protocol: Three samples were placed in an environment at 40°C (RH= 75%) for 7 consecutive days, sampled every other day, and PCC1 content changes were monitored using HPLC to calculate degradation rates.
PCC1-Enriched Phytosomal Formulation improves the stability of PCC1
Chart showing retention rates over 7 days comparing PCC1, PCC1-Enriched Lecithin (Soy), and PCC1-Enriched Lecithin (Egg-Yolk) formulations, demonstrating superior stability of encapsulated forms.

Higher Retention During Digestion

The formulation mitigates the direct degradation of PCC1 by gastric acid and digestive enzymes, facilitating its gradual release upon reaching the small intestine. This controlled release mechanism prevents concentrated exposure or rapid degradation within a short timeframe, allowing PCC1 to effectively navigate the "degradation corridor" while maintaining elevated levels of bioavailable compound.

Post-phytosomal digestion, PCC1 retention is measured at 84%, significantly higher than the baseline of approximately 58–59% observed with unencapsulated PCC1, representing a relative increase of approximately 44%.

Experimental Protocol: A modified mouse in vitro gastrointestinal digestion model was used: samples were first subjected to gastric conditions (pH 2.5, pepsin, 37°C, 60 min) and then transferred to intestinal conditions (pH 6.8, pancreatin + bile salts, 37°C, 90 min). After termination, residual content was measured as a percentage of the initial value (Mean±SD, n=3)
Stability of Extracorporeal Gastrointestinal Digestion
Bar chart comparing Initial Content, Gastric Digestion, and Intestinal Digestion retention rates for PCC1, PCC1-Enriched Lecithin (Soy), and PCC1-Enriched Lecithin (Egg-Yolk), showing superior digestive stability of phytosomal formulations.

Enhancement in Oral Bioavailability

Phospholipids, structurally analogous to intestinal mucosal membrane components, significantly facilitate the uptake and transport of PCC1-enriched lecithin within the gastrointestinal tract. The optimized particle size and phospholipid interface synergistically enhance dissolution and dispersion, thereby accelerating the initial absorption rate.

Furthermore, our PCC1-formulation ensures a balanced release profile, effectively prolonging the high-concentration maintenance interval. Remarkably, the blood peak concentration of PCC1 polyphenols in the phytosomal group is 2.6 times higher than that of the conventional form. Additionally, the time to reach peak blood concentration following oral administration is substantially reduced, while the extended high-concentration maintenance interval further underscores the superior bioavailability and sustained efficacy of the phytosomal formulation.

Experimental Protocol: 9 male mice were randomly divided into 3 groups and orally administered PCC1 and its soybean/egg yolk lecithin preparations, with a single PCC1 dose of 20 mg/kg in each formulation. Blood samples were collected every 5 minutes after administration, centrifuged at 3000 rpm for 10 minutes, and supernatants (lithium heparin) were stored at -20°C for analysis.
PCC1-Enriched Phytosomal Formulation improves oral absorption efficacy
Absorption curve chart showing blood concentration over time (0-80 minutes) comparing PCC1, PCC1-Enriched Lecithin (Soy), and PCC1-Enriched Lecithin (Egg-Yolk), demonstrating superior bioavailability of phytosomal formulations.

Overall Performance Summary

Compared to traditional free-state PCC1, the encapsulated PCC1-Phytosomal formulation demonstrates significantly enhanced biocompatibility and delivery precision. In addition, PCC1 formulations prepared using pharmaceutical-grade egg yolk lecithin demonstrate significantly superior performance compared to those made with plant-derived lecithin. Our innovative technological advancement provides a robust foundation for the development of high-end functional nutrition products. These improvements highlight the potential of the phytosomal formulation to maximize the bioavailability and therapeutic efficacy of PCC1 in vivo.

Key Performance Metrics Include:

93%
Stability Retention
84%
Digestive Retention
2.6×
Faster Absorption Peak
Extended
Active Duration

Compliance Notice

The above descriptions are based on the general scientific properties of procyanidin substances and internal in vitro/animal model data trends. They do not directly equate to human efficacy conclusions. Not intended for disease prevention, diagnosis, or treatment. Actual claims should comply with local regulations and subsequent clinical/population observational data.