In cancer patients, metastasis begins when cells at the primary tumour switch from a stable, cohesive state to an invasive one driven principally by hypoxia, inflammation and a stiffening, fibrotic stroma. Hypoxia stabilises HIF-1α, and together with TGF-β, Wnt and NF-κB signalling this activates EMT transcription factors (Snail, Twist, ZEB1). These repress E-cadherin, so cells lose adhesion to neighbours, gain a mesenchymal, motile phenotype, and acquire stem-like and survival traits. At the same time, the cells remodel their surroundings. MMPs, uPA and cathepsins degrade the basement membrane, while LOX stiffens the collagen matrix. Integrin-FAK-Src and Rho/Rac signalling then reorganise the actin cytoskeleton so the cells can crawl through the matrix toward blood and lymphatic vessels. Tumour-derived VEGF creates leaky, abnormal vessels, and chemokine gradients (CXCL12/CXCR4, CCL2) draw cells toward them. Metaxin is proprietarily formulated to target HIF-1α/TGF-β/Wnt/NF-κB axes, its components also disrupt MMPs and inhibit PD/PDL1 for enhanced immune-surveillance.
Myofibrox is a proprietary blend of four herbs with definitive action on four key pathological drivers of uterine fibroids. The first component antagonizes progesterone/PR-A/PR signaling. The second component is a dual inhibitor of intratumoral aromatase and 17β-HSD1.
Prostafexin is a scientifically validated and standardized herbal formulation already established for centuries. One of the components achieve dual 5α-reductase/PDE5 inhibition thus, countering the ED effect of 5α-reductase inhibition. Another component specifically blocks α1A-adrenoceptor signalling, causing relaxation of the smooth muscle tissue in the prostate and bladder neck, thus, improving urinary flow and reduces lower urinary tract symptoms.
Beyond any tissue-specific proliferative signals that drives oncogenesis, all pathways must ultimately cascade to cell-cycle; thus, our proprietary Atxilox is a carefully blended botanicals which specifically inhibits CDK4/6-cyclin D-Rb, recovers mitochondrial apoptosis evasion via Bcl-2/Bcl-xL/Mcl-1, XIAP/survivin downregulation and blockage of VEGF/VEGFR angiogenesis which sustains tumour vasculature.
