| Features: | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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/
|
| Source: |
| Type: |
| -An enzyme complex that plays a crucial role in cellular metabolism, particularly in the conversion of pyruvate to acetyl-CoA, which is then used to produce energy in the form of ATP.
-Key enzyme in cellular metabolism that catalyzes the conversion of pyruvate (produced during glycolysis) into acetyl-CoA, which then enters the tricarboxylic acid (TCA) cycle in the mitochondria. The phosphorylation state of PDH (p-PDH) broadly exists in the cancer cells. Some cancer cells have been found to inhibit PDH activity, which can lead to increased lactate production and a shift towards glycolysis, even in the presence of oxygen. This is known as the Warburg effect. -In cancer cells, PDH has been shown to be inhibited. PDH expression is regulated by various transcription factors, including HIF-1α, c-Myc, and p53. |
| 5196- | DCA, | Dichloroacetate induces apoptosis in endometrial cancer cells |
| - | in-vitro, | Var, | NA |
| 1882- | DCA, | Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer |
| - | Analysis, | NA, | NA |
| 1864- | DCA, | MET, | Dichloroacetate Enhances Apoptotic Cell Death via Oxidative Damage and Attenuates Lactate Production in Metformin-Treated Breast Cancer Cells |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | T47D | - | in-vitro, | Nor, | MCF10 |
| 1867- | DCA, | Chemo, | Sensitization of breast cancer cells to paclitaxel by dichloroacetate through inhibiting autophagy |
| - | in-vivo, | BC, | NA | - | in-vitro, | BC, | NA |
| 1866- | DCA, | MET, | BTZ, | Targeting metabolic pathways alleviates bortezomib-induced neuropathic pain without compromising anticancer efficacy in a sex-specific manner |
| - | in-vivo, | NA, | NA |
| 2044- | PB, | DCA, | Differential inhibition of PDKs by phenylbutyrate and enhancement of pyruvate dehydrogenase complex activity by combination with dichloroacetate |
| - | in-vivo, | NA, | NA |
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:288 Target#:245 State#:% Dir#:2
wNotes=0 sortOrder:rid,rpid