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| Dichloroacetate (DCA) is a metabolic modulator that targets the altered metabolic state of cancer cells by inhibiting PDKs. This action impacts several key pathways: • Reversal of the Warburg effect • Restoration of mitochondrial function and promotion of apoptosis • suppresses glycolysis and promotes oxidative phosphorylation, thereby increasing mitochondrial ROS-mediated apoptosis in tumor cells • Increase in ROS production leading to oxidative stress • Inhibition of cell cycle progression • Modulation of HIF-1α signaling: DCA might decrease HIF-1α stabilization, thereby reducing the expression of genes that support glycolysis, angiogenesis, and survival under low-oxygen conditions. -DCA has been primarily used in treating congenital lactic acidosis—a rare genetic disorder characterized by the buildup of lactic acid in the body. -DCA is an anti-diabetic and lipid-lowering drug, as well as treating myocardial and cerebrovascular ischemia. -Do not add DCA to hot or warm beverages. DCA is unstable at higher temperatures -Caffeinated increases effectiveness -Vitamin B1 reduces neuropathy (500mg-2500mg/day) -Possibly 20 grams of citric acid 20 minutes before taking DCA -Procaine, Diclofenac or Sulindac to increase SMCT1 -Omeprazole 80mg/day to increase DCA effectiveness -Scorpion venom to increase DCA effectiveness -Metformin 1000mg to 1500mg/day -Propranolol (Ref.) -Fenbendazole shows strong synergy when combined to DCA, So it may make very much sense to combine the two. "Note: DCA is not tumor cell specific,> and therefore the same shift in glucose metabolism that occurs in cancer cells will also take place in immune cells, leading to induction of Tregs (Ref.). In order to avoid this possibility, while using DCA I would also use Treg inhibitors such as Cimetidine (Ref.) or low dose Cyclophosphamide (Ref.)." Dose: 10mg/kg/day and increase slowly to about 25mg/kg/day:(1/2morn,1/2evening) take 5 days on, 2 off? OR 2wks on/ 1wk off: https://www.thedcasite.com/dca_dosage.html Done by mixing it in water and drinking, suggested that DCA not be taken on an empty stomach. **** DCA-induced apoptosis in cancer cells requires sodium-coupled monocarboxylates transporter SLC5A8 (SMCT1) -Inhibitors of DNA methylation induce reactivation of SLC5A8 -Procaine is a DNA-demethylating agent with growth-inhibitory effects in human cancer cells. -SMCT1 was found to be stimulated by some other NSAIDs (diclofenac, meclofenamate and sulindac), by activin A143 and by the probiotic Lactobacillus plantarum. SMCT1 has been found to be inhibited by some NSAIDs (ibuprofen, ketoprofen, fenoprofen, naproxen135 and indomethacin94), phytochemicals (resveratrol and quercetin) **** Hence these should be avoided with DCA. (also AVOID Bromide, iodide and sulfite ) **** GSTZ1 an/or chloride anion transport inhibitors also reduce resistance to DCA (if the tumor expresses GSTZ1 and contains a high chloride anions level, the GSTZ1 will be stable, maintaining the resistance to DCA). -Dichloroacetate-dca-treatment-strategy GSTZ1 an/or chloride anion transport inhibitors. . -Etacrynic acid is a Cl(-)-ATPase inhibitor -Lansoprazole and Omeprazole inhibit chloride channels. -Chlorotoxin found in scorpion venom (see my post on scorpion venom) can also inhibit chlorine channels Sources: https://northernhealthproducts.com/shop/ https://www.dcalab.com/
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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 4901- | DCA, | Sal, | Dichloroacetate and Salinomycin as Therapeutic Agents in Cancer |
| - | Review, | NSCLC, | NA |
| 1878- | DCA, | 5-FU, | Synergistic Antitumor Effect of Dichloroacetate in Combination with 5-Fluorouracil in Colorectal Cancer |
| - | in-vitro, | CRC, | LS174T | - | in-vitro, | CRC, | LoVo | - | in-vitro, | CRC, | SW-620 | - | in-vitro, | CRC, | HT-29 |
| 1874- | DCA, | Dichloroacetate induces apoptosis of epithelial ovarian cancer cells through a mechanism involving modulation of oxidative stress |
| - | in-vitro, | Ovarian, | SKOV3 | - | in-vitro, | Ovarian, | MDAH-2774 |
| 1888- | VitB1/Thiamine, | DCA, | High Dose Vitamin B1 Reduces Proliferation in Cancer Cell Lines Analogous to Dichloroacetate |
| - | in-vitro, | PC, | SK-N-BE | - | NA, | PC, | PANC1 |
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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