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| rMETase - Recombinant Methioninase Recommended Abbreviation: rMETase Alternative Names: Recombinant methioninase, recombinant L-methionine α-deamino-γ-mercaptomethane lyase, recombinant methionine γ-lyase Type: Recombinant enzyme / metabolic anticancer therapy / methionine-depleting biologic Source: Recombinant methioninase is commonly produced from the Pseudomonas putida methioninase gene expressed in Escherichia coli. Function: rMETase enzymatically degrades methionine and lowers extracellular and systemic methionine availability. Many cancer cells display methionine dependence or methionine addiction and therefore cannot maintain proliferation when extracellular methionine is depleted, whereas normal cells are generally more capable of compensating through methionine regeneration and related metabolic pathways. Cancer: Preclinical studies demonstrate broad anticancer activity through methionine depletion, inhibition of proliferation, disruption of methylation-dependent metabolism, and cell-cycle arrest, frequently in late S/G2 phase. rMETase can sensitize cancer cells to chemotherapy and has shown synergistic activity with multiple cytotoxic agents in experimental tumor models. Clinical Status: Experimental metabolic anticancer therapy. Most evidence is preclinical, although recombinant methioninase has been developed specifically for translational and clinical investigation. |
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| The selectivity of cancer products (such as chemotherapeutic agents, targeted therapies, immunotherapies, and novel cancer drugs) refers to their ability to affect cancer cells preferentially over normal, healthy cells. High selectivity is important because it can lead to better patient outcomes by reducing side effects and minimizing damage to normal tissues. Achieving high selectivity in cancer treatment is crucial for improving patient outcomes. It relies on pinpointing molecular differences between cancerous and normal cells, designing drugs or delivery systems that exploit these differences, and overcoming intrinsic challenges like tumor heterogeneity and resistance Factors that affect selectivity: 1. Ability of Cancer cells to preferentially absorb a product/drug -EPR-enhanced permeability and retention of cancer cells -nanoparticle formations/carriers may target cancer cells over normal cells -Liposomal formations. Also negatively/positively charged affects absorbtion 2. Product/drug effect may be different for normal vs cancer cells - hypoxia - transition metal content levels (iron/copper) change probability of fenton reaction. - pH levels - antiOxidant levels and defense levels 3. Bio-availability |
| 8033- | IVM, | dietMet, | rMETase, | Direct comparison of efficacy of combining ivermectin versus five first-line chemotherapy drugs with recombinant methioninase against colon-cancer cells |
| - | in-vitro, | CRC, | HCT116 |
| - | in-vitro, | Lung, | A549 |
| 8052- | IVM, | rMETase, | Selective Synergy of Ivermectin Combined With Recombinant Methioninase Against Colon-Cancer Cells in Contrast to Normal Fibroblasts |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | Nor, | Hs27 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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