A1 MarkII

A1 MarkII

$112.90
PAN16-A1

Complex blend of immunomodulating botanicals with multiple anticancer activities including: - inhibiting angiogenesis, modulating p53 and VEGF, lowering proinflammatory cytokines and modulating imbalance of Th1/Th2.*

Supplement Facts

Serving Size: 15 gm

Servings Per Container: 40

Amount Per Serving

% Daily Value
Astragalus (root) (Huang Qi) 2.3 g †
Ligustrum (fruit) (Nu zhen zi) 0.86 g †
Asian Ginseng (root) (Ren Shen) 0.57 g †
Turmeric (rhizome) (Yu Jin)) 0.57 g †
Reishi (fruiting body) (Ling Zhi) 0.28 g †
Gynostemma (above ground parts) (Jiao Gu Lan) 0.28 g †
Bai zhu atractylodes (rhizome) (Bai Zhu) 0.86 g †
Barbed skullcap (whole plant) (Ban Zhi Lian) 1.15 g †
Hedyotis (whole plant) (Bai Hua She Cao) 2.30 g †
Poria (sclerotium) (Fu Ling) 0.86 g †
Eupolyphaga sinensis (Tu Bei Chong) 0.57 g †
Endothelium Corneum Gigeriae Galli (Ji Nei Jin) 0.57 g †
Duchesnea indica (whole plant) (She Mei) 0.86 g †
Solanum lyratum (whole herb) (Bai Ying Cao) 1.15 g †
Yin-chen wormwood (young shoot) (Yin Chen) 1.15 g †
Cynanchum Paniculatum (root) (Xu Chang Qing) 0.57 g †
† Daily Value not established.

Other Ingredients: Starch (rice)

Does Not contain: Wheat, gluten, soy, milk, eggs, fish, crustacean shellfish, tree nuts, peanuts

A1-Mark II

600 Grams

Product Overview

A1 Mark II formulation is a combination of traditional herbs used to support during times of intense physiological challenge. Physiological challenges are consistent with changes in all aspects of human functioning and underlies multiple systemic biomedical changes. Prolonged challenge and associated physical weakness trigger a cascade of cellular and physical responses. Ginseng and Gynostemma combined with additional herbs have been used for centuries to support optimum strength and vitality throughout periods of intense physical and physiological challenge.*

Actions  

• Supports healthy cell cycle regulation*

• Inhibits oxidative damage*

• Promotes normal cellular behavior*

• Supports healthy immune response* 

Suggested Use: 

15 Grams x 2 times daily. Dissolve granules in hot water

Caution: 

None noted

Warning: 

None Noted

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

A1-Mark II (Yangzheng Xiaoji) is a traditional Chinese medical formulation that has been shown to have anticancer actions in patients with various solid tumours.

The mechanisms of the potential anticancer action of A1-Mark II are unknown. In the present study, Ye et al., (2012) investigated the direct effects of A1-Mark II on a range of human cancer cell lines and investigated the possible mechanism(s) of its action. An extract of A1-Mark II (DME25) was prepared using dimethyl sulfoxide. The influence of DME25 on in vitro growth, adhesion and migration was examined using in vitro function assays. The effects on signalling protein kinases were assessed using western blotting.*

DME25 suppressed adhesion and migration of various cancer cell, including those of breast, prostate, lung, osteosarcoma and colorectal cancer. Further investigation showed an involvement of the phosphatidylinositol 3-kinases/protein kinase B (PI3K/AKT) pathway in the inhibitory effect on the adhesion of cancer cells by DME25.*

A1-Mark II exerts its anticancer effects not only via synergistically working together with chemotherapy, but also by directly inhibiting adhesion and migration of cancer cells. The PI3K/AKT pathway is a potential signalling pathway targeted by A1-Mark II.*

The effect of A1-Mark II on the activation of focal adhesion kinase (FAK) and paxillin was evaluated by immunofluorescence methods. It was found that A1-Mark II exhibited a significant inhibitory effect on cell-matrix adhesion as demonstrated by a cell-based assay and electric cell-substrate impedance sensing (ECIS) analysis. The effect was observed together with a reduction in phospho-FAK and phospho-paxillin in the cells when treated with A1-Mark II. In the in vivo tumour model, A1-Mark II was found to significantly inhibit the growth of osteosarcoma with a sustained effect observed when A1-Mark II was delivered intraperitoneally. A1-Mark II sensitized cells to the effect of FAK inhibitor in vitro and in vivo. It is concluded that A1-Mark II plays a significant role in cell-matrix adhesion and tumour growth, likely by inhibiting the activation of the FAK pathway. The therapeutic role of A1-Mark II in osteosarcoma warrants further investigation (Jiang et al., 2013).*

References

Jiang WG, Ye L, Ji K, Frewer N, Ji J, Mason MD. Inhibitory effects of Yangzheng Xiaoji on angiogenesis and the role of the focal adhesion kinase pathway. Int J Oncol. 2012 Nov;41(5):1635-42. doi: 10.3892/ijo.2012.1627.

Jiang WG, Ye L, Ji K, Ruge F, Wu Y, Gao Y, Ji J, Mason MD. Antitumour effects of Yangzheng Xiaoji in human osteosarcoma: the pivotal role of focal adhesion kinase signalling. Oncol Rep. 2013 Sep;30(3):1405-13. doi: 10.3892/or.2013.2586.

Ye L, Ji K, Frewer N, Ji J, Jiang WG. Impact of Yangzheng Xiaoji on the adhesion and migration of human cancer cells: the role of the AKT signalling pathway. Anticancer Res. 2012 Jul;32(7):2537-43.

Inhibitory effects of Yangzheng Xiaoji on angiogenesis and the role of the focal adhesion kinase pathway 

Wen G. Jiang, Lin Ye, Ke Ji, Natasha Frewer, Jiafu Ji, Malcolm D. Mason. International Journal Of Oncology 41: 1635-1642, 2012m DOI: 10.3892/ijo.2012.1627 

DME25 (A1-Mark II) inhibited formation of microvessel-like tubules without affecting the growth of endothelial cells

Using an in vitro tubule formation assay, it was shown that DME25 significantly reduced tubule length compared with control (p=0.046). This was seen at concentrations at which no growth inhibition was achieved at the concentrations without cytotoxicity on HECV cells. DME25 over a wide concentration did not have a significant influence on the growth of endothelial cells*

DME25 (A1-Mark II) exerted an inhibitory effect on cell-matrix adhesion

DME25 demonstrated a concentration-dependent inhibitory effect on the adhesion of HECV cells, with marked inhibitory effects seen at dilutions of 1:5,000 or lower. Using 3D modelling, it was seen that the inhibitory effects by DME25 were seen across the frequencies tested. Using conventional cell-matrix adhesion method, DME25 had a significant inhibitory effect on the adhesion.*

Endothelial cell migration was reduced by DME25 (A1-Mark II)

In a similar fashion to cell-matrix adhesion, cellular migration was similarly inhibited by the presence of DME25 and was further inhibited when FAK inhibitor was used together with DME25.*

DME25 (A1-Mark II) and FAK inhibitor had a synergistic effect on the adhesion, migration and tubule formation of endothelial cells

FAK inhibitor has a marked effect on the adhesion of HECV cells. When administered together with DME25, the inhibitory effect appears to be synergistically strengthened.*

FAK inhibitor appears to have an inhibitory effect on tubule formation although this is not statistically significant (p=0.14). However, the combination between DME25 and FAK inhibitor had a marked inhibition on tubule formation, compared with control, with FAK inhibitor along and DME25 along (p=0.006, p=0.041, p=0.011, respectively).*

DME25 (A1-Mark II) inhibited phosphorylation of FAK in endothelial cells

We further evaluated the effect of DME25 on the activation of FAK and paxillin in HECV cells, namely tyrosine phophorylation in these proteins, using phospho-tyrosine specific antibodies.DME25 suppressed phosphorylation of FAK and produced more profound inhibition together with FAK inhibitor. Neither DME25 nor FAK inhibitor or their combinations had marked effect on the phosphorylation of paxillin.*

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.