Colorectal adenocarcinoma marker inhibitors are a class of chemical compounds designed to specifically target and inhibit the activity of proteins or molecular markers that are predominantly expressed in colorectal adenocarcinoma cells. Colorectal adenocarcinoma, a type of cancer that originates in the epithelial cells lining the colon or rectum, is characterized by the overexpression or mutation of various biomarkers that contribute to the malignant behavior of these cells, including their growth, proliferation, and survival. These biomarkers can include a variety of proteins such as specific enzymes, growth factors, receptors, and transcription factors that are involved in signaling pathways driving the development and progression of colorectal adenocarcinoma. Inhibitors targeting these markers are designed to interfere with their activity or expression, thereby disrupting the pathways and processes that sustain the cancerous phenotype of the cells.
The development of colorectal adenocarcinoma marker inhibitors involves extensive research to identify and characterize the key molecular markers associated with this type of cancer. Once these markers are identified, structural studies are conducted to determine the precise binding sites and functional domains within these proteins that can be targeted by inhibitors. These inhibitors may take the form of small molecules, peptides, or antibodies that bind specifically to the target markers, blocking their function or leading to their degradation. By inhibiting these markers, the compounds can alter the signaling pathways that these proteins regulate, potentially affecting processes such as cell division, apoptosis, and angiogenesis. The specificity of these inhibitors is crucial, as many of the biomarkers involved in colorectal adenocarcinoma may also be present in normal tissues, albeit at lower levels. Therefore, the inhibitors are designed to selectively target the cancer-associated forms or levels of these markers to minimize off-target effects. Advanced techniques such as molecular modeling, high-throughput screening, and structure-activity relationship studies are utilized to optimize the binding affinity and selectivity of these inhibitors, ensuring that they effectively target colorectal adenocarcinoma markers without affecting normal cellular functions.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Fluorouracil | 51-21-8 | sc-29060 sc-29060A | 1 g 5 g | $36.00 $149.00 | 11 | |
Through its metabolite, FdUMP, Fluorouracil directly inhibits thymidylate synthase, leading to a decrease in thymidine monophosphate and subsequent DNA synthesis arrest. This could downregulate markers associated with colorectal adenocarcinoma due to reduced proliferation of cancer cells. | ||||||
Oxaliplatin | 61825-94-3 | sc-202270 sc-202270A | 5 mg 25 mg | $110.00 $386.00 | 8 | |
Oxaliplatin forms platinum-DNA adducts, which compromise DNA replication and transcription. This action can lead to cell cycle arrest and apoptosis, potentially decreasing the level of markers indicative of colorectal adenocarcinoma. | ||||||
(+)-Irinotecan | 97682-44-5 | sc-269253 | 10 mg | $61.00 | 1 | |
By binding to the topoisomerase I-DNA complex, Irinotecan prevents DNA relegation, causing DNA damage and cell death, which can lower the levels of specific colorectal adenocarcinoma markers due to reduced tumor cell viability. | ||||||
Curcumin | 458-37-7 | sc-200509 sc-200509A sc-200509B sc-200509C sc-200509D sc-200509F sc-200509E | 1 g 5 g 25 g 100 g 250 g 1 kg 2.5 kg | $36.00 $68.00 $107.00 $214.00 $234.00 $862.00 $1968.00 | 47 | |
Curcumin has been shown to downregulate the expression of various genes involved in proliferation, apoptosis, and angiogenesis, which could lead to a reduction in the levels of colorectal adenocarcinoma markers. | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Resveratrol has been found to inhibit the proliferation of various cancer cell lines, which could translate to a decrease in the expression of colorectal adenocarcinoma markers through the induction of cell cycle arrest and apoptosis. | ||||||
Sulindac | 38194-50-2 | sc-202823 sc-202823A sc-202823B | 1 g 5 g 10 g | $31.00 $84.00 $147.00 | 3 | |
As a precursor to an active sulfide metabolite that inhibits both COX-1 and COX-2, Sulindac could reduce the synthesis of pro-inflammatory prostaglandins, potentially leading to a reduction in colorectal adenocarcinoma marker levels. | ||||||
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 induce cell cycle arrest and promote apoptosis in various cancer cells, potentially resulting in the downregulation of colorectal adenocarcinoma markers due to decreased cell viability. | ||||||
(−)-Epigallocatechin Gallate | 989-51-5 | sc-200802 sc-200802A sc-200802B sc-200802C sc-200802D sc-200802E | 10 mg 50 mg 100 mg 500 mg 1 g 10 g | $42.00 $72.00 $124.00 $238.00 $520.00 $1234.00 | 11 | |
Epigallocatechin Gallate inhibits several key molecules involved in signal transduction and cell cycle progression, which may lead to a reduction in colorectal adenocarcinoma marker levels by hindering cancer cell growth and inducing apoptosis. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $62.00 $155.00 $320.00 | 233 | |
Rapamycin is a known inhibitor of mTOR, a central cell growth regulator. By inhibiting mTOR, Rapamycin can decrease protein synthesis and cell proliferation, potentially leading to lowered levels of colorectal adenocarcinoma markers. | ||||||
Aspirin | 50-78-2 | sc-202471 sc-202471A | 5 g 50 g | $20.00 $41.00 | 4 | |
Aspirin's inhibition of COX enzymes could lead to a decrease in the biosynthesis of prostaglandins, which are involved in tumor growth and inflammation, potentially leading to reduced colorectal adenocarcinoma marker levels. | ||||||