Chemical inhibitors of SCOCO can operate through various mechanisms to disrupt its function within cellular metabolic pathways. Phloretin, a known inhibitor of glucose transporters, can indirectly inhibit SCOCO by reducing the intracellular availability of glucose, which is the primary substrate for glycolysis. As SCOCO is involved in glycolytic processes, the reduced availability of glucose results in a deficiency of glycolytic intermediates, which are essential for SCOCO's activity. Similarly, 2-Deoxy-D-glucose competitively inhibits hexokinase, leading to a reduction in the production of glycolytic intermediates and thereby limiting SCOCO's function. Lonidamine also targets hexokinase, further compounding the decrease in glycolytic flux and indirectly inhibiting SCOCO's glycolytic role. 3-Bromopyruvate alkylates and inhibits glycolytic enzymes, which diminishes the metabolic flux through glycolysis, thus reducing the availability of substrates required for SCOCO's activity.
The inhibition of various enzymes in the glycolytic pathway by chemicals like Iodoacetate, which irreversibly inhibits glyceraldehyde-3-phosphate dehydrogenase, disrupts the formation of downstream metabolites that SCOCO may utilize, indirectly inhibiting its metabolic functions. Oxamate's inhibition of lactate dehydrogenase can alter the cellular redox state and reduce NAD+ regeneration, which is crucial for glycolysis and thus SCOCO's activity. Compounds such as α-Cyano-4-hydroxycinnamate inhibit the mitochondrial pyruvate carrier, potentially decreasing pyruvate availability for SCOCO's metabolic pathways. The inhibition of protein phosphorylation by Genistein can indirectly inhibit SCOCO due to the role of phosphorylation in regulating metabolic enzymes and proteins that interact with SCOCO. Quercetin's inhibition of PI3K signaling can disrupt cellular energy balance and metabolic regulation, which can also functionally inhibit SCOCO's role in metabolism. Lastly, inhibitors of mitochondrial electron transport, such as Rotenone and Antimycin A, reduce ATP availability and alter redox states, which can indirectly inhibit SCOCO by affecting the metabolic pathways and energy homeostasis that are central to its function.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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Phloretin | 60-82-2 | sc-3548 sc-3548A | 200 mg 1 g | $63.00 $250.00 | 13 | |
Phloretin is known to inhibit glucose transporters (GLUTs). As SCOCO is implicated in glycolysis and interacts with components of the cellular metabolism, inhibition of glucose transport can decrease the availability of glycolytic intermediates, thereby functionally inhibiting SCOCO by limiting its metabolic substrate. | ||||||
2-Deoxy-D-glucose | 154-17-6 | sc-202010 sc-202010A | 1 g 5 g | $65.00 $210.00 | 26 | |
2-Deoxy-D-glucose is a glucose analog that inhibits glycolysis by interfering with hexokinase. As SCOCO is associated with glycolytic processes, the inhibition of hexokinase can lead to a reduction in glycolytic intermediates, thereby indirectly inhibiting the functional activity of SCOCO. | ||||||
Lonidamine | 50264-69-2 | sc-203115 sc-203115A | 5 mg 25 mg | $103.00 $357.00 | 7 | |
Lonidamine inhibits hexokinase, an enzyme crucial for the initiation of glycolysis. By inhibiting hexokinase, lonidamine would decrease the production of glycolytic intermediates required for SCOCO's metabolic functions, resulting in its functional inhibition. | ||||||
Iodoacetic acid | 64-69-7 | sc-215183 sc-215183A | 10 g 25 g | $56.00 $97.00 | ||
Iodoacetate irreversibly inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in glycolysis. As SCOCO is involved in metabolic pathways, the inhibition of GAPDH would disrupt glycolytic flow, indirectly inhibiting SCOCO's associated metabolic activities. | ||||||
Sodium dichloroacetate | 2156-56-1 | sc-203275 sc-203275A | 10 g 50 g | $54.00 $205.00 | 6 | |
Dichloroacetate stimulates pyruvate dehydrogenase activity, shifting cellular metabolism from glycolysis to oxidative phosphorylation. This shift can reduce the metabolic intermediates that SCOCO may utilize, thereby functionally inhibiting SCOCO's role in glycolysis. | ||||||
Oxamic acid | 471-47-6 | sc-250620 | 25 g | $145.00 | ||
Oxamate is a competitive inhibitor of lactate dehydrogenase (LDH). Inhibition of LDH could decrease the regeneration of NAD+ from NADH, thus altering the redox state and metabolic intermediates in glycolysis where SCOCO is active, leading to its functional inhibition. | ||||||
α-Cyano-4-hydroxycinnamic acid | 28166-41-8 | sc-254923 | 2 g | $42.00 | 2 | |
This compound inhibits the mitochondrial pyruvate carrier, which could decrease the availability of pyruvate for mitochondrial metabolism, potentially disrupting the metabolic balance and indirectly inhibiting the function of SCOCO in metabolic pathways. | ||||||
Genistein | 446-72-0 | sc-3515 sc-3515A sc-3515B sc-3515C sc-3515D sc-3515E sc-3515F | 100 mg 500 mg 1 g 5 g 10 g 25 g 100 g | $26.00 $92.00 $120.00 $310.00 $500.00 $908.00 $1821.00 | 46 | |
Genistein is a tyrosine kinase inhibitor that can inhibit the phosphorylation of proteins involved in various signaling pathways. As phosphorylation can regulate the function of metabolic enzymes and proteins, it can indirectly inhibit SCOCO by altering its phosphorylation state and interaction with other proteins. | ||||||
Quercetin | 117-39-5 | sc-206089 sc-206089A sc-206089E sc-206089C sc-206089D sc-206089B | 100 mg 500 mg 100 g 250 g 1 kg 25 g | $11.00 $17.00 $108.00 $245.00 $918.00 $49.00 | 33 | |
Quercetin is known to inhibit phosphoinositide 3-kinases (PI3Ks). By inhibiting PI3K, quercetin can alter the signaling pathways that regulate metabolism and cellular energy balance, which may lead to the functional inhibition of SCOCO by disrupting its metabolic context. | ||||||
Rotenone | 83-79-4 | sc-203242 sc-203242A | 1 g 5 g | $89.00 $254.00 | 41 | |
Rotenone is an inhibitor of mitochondrial complex I. By inhibiting complex I, rotenone can reduce the availability of ATP and alter the cellular energetic state, which could indirectly inhibit the function of SCOCO by affecting its metabolic interactions. |