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. A patient on Atxilox is also treated with Sphenolax and Nu-beta, these formulations jointly reverse Warburg metabolic effect and dyslipidemia. Since our preparation method is aimed at preserving the flavonoid-class within other key target phytochemicals, Inflammation and redox imbalance associated with carcinogenesis is blocked by the flavonoid-rich fraction via NF-κB/STAT3/COX-2/PGE₂/ROS pathways. Thus, Atxilox reduces tumour volume, and ultimately promotes patient survival as a single agent, and when combined with chemotherapy, it mitigates against therapy resistance.
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.
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.
