Items 101 to 110 of 261 total
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
PGJ2 (Prostaglandin J2) | 60203-57-8 | sc-201248 sc-201248A sc-201248B sc-201248C sc-201248D | 1 mg 10 mg 50 mg 100 mg 500 mg | $228.00 $1857.00 $9180.00 $13770.00 $64566.00 | ||
PGJ2, a bioactive prostaglandin, exhibits potent antineoplastic properties through its unique ability to activate peroxisome proliferator-activated receptors (PPARs). This activation modulates gene expression involved in cell proliferation and apoptosis. PGJ2 also interacts with various signaling pathways, influencing oxidative stress responses and inflammation. Its electrophilic nature allows it to form covalent bonds with specific cysteine residues in proteins, altering their function and contributing to its biological effects. | ||||||
Carmofur | 61422-45-5 | sc-204670 sc-204670A | 1 g 5 g | $102.00 $437.00 | 3 | |
Carmofur is a synthetic compound that exhibits antineoplastic activity by inhibiting key enzymes involved in nucleotide synthesis, thereby disrupting DNA replication in cancer cells. Its unique structure allows for selective interaction with cellular targets, leading to the modulation of apoptotic pathways. Additionally, Carmofur's ability to generate reactive oxygen species enhances its cytotoxic effects, promoting oxidative stress within tumor cells and contributing to its overall efficacy in cancer treatment. | ||||||
Amonafide | 69408-81-7 | sc-207283 | 10 mg | $216.00 | 2 | |
Amonafide is a synthetic antineoplastic agent characterized by its ability to intercalate into DNA, disrupting the double helix structure and inhibiting topoisomerase II activity. This interference with DNA topology leads to the accumulation of DNA breaks, triggering cellular stress responses. Amonafide's unique molecular interactions also promote the generation of reactive intermediates, enhancing its cytotoxic potential and influencing cellular signaling pathways associated with apoptosis. | ||||||
Pirarubicin | 72496-41-4 | sc-205810 sc-205810A | 5 mg 10 mg | $170.00 $300.00 | ||
Pirarubicin is a potent antineoplastic compound that exhibits unique interactions with cellular components, particularly through its ability to form stable complexes with DNA. This interaction leads to the stabilization of the DNA double helix, ultimately resulting in the inhibition of DNA replication and transcription. Additionally, Pirarubicin induces oxidative stress within cells, promoting the generation of reactive oxygen species that can further disrupt cellular homeostasis and enhance its cytotoxic effects. | ||||||
7-Ethyl Camptothecin | 78287-27-1 | sc-207171 | 10 mg | $278.00 | ||
7-Ethyl Camptothecin is a distinctive antineoplastic agent characterized by its ability to inhibit topoisomerase I, an enzyme crucial for DNA unwinding during replication. This inhibition leads to the formation of DNA breaks, preventing proper cell division. The compound's unique lactone structure enhances its affinity for the enzyme, facilitating a prolonged interaction that disrupts the normal cellular repair mechanisms. Its selective targeting of rapidly dividing cells underscores its potential in modulating cellular dynamics. | ||||||
A-7 hydrochloride | 79127-24-5 | sc-203794A sc-203794 | 5 mg 10 mg | $102.00 $122.00 | 2 | |
A-7 hydrochloride exhibits unique properties as an antineoplastic agent through its interaction with cellular signaling pathways. It selectively binds to specific receptors, modulating downstream effects that influence cell cycle progression. The compound's ability to alter gene expression profiles enhances its efficacy in disrupting tumor growth. Additionally, its stability in aqueous environments allows for sustained activity, making it a noteworthy candidate for further exploration in cellular response mechanisms. | ||||||
cis-trismethoxy Resveratrol | 94608-23-8 | sc-205255 sc-205255A | 10 mg 50 mg | $24.00 $108.00 | ||
Cis-trismethoxy Resveratrol demonstrates intriguing behavior as an antineoplastic compound by engaging in redox reactions that influence oxidative stress within cells. Its unique methoxy groups enhance lipophilicity, facilitating membrane permeability and subsequent intracellular interactions. This compound also exhibits a capacity to inhibit key enzymes involved in tumor metabolism, potentially altering energy production pathways. Its structural conformation allows for effective stacking interactions with DNA, contributing to its role in modulating cellular proliferation. | ||||||
7-epi-Taxol | 105454-04-4 | sc-202894B sc-202894C sc-202894 sc-202894A | 500 µg 1 mg 5 mg 10 mg | $70.00 $115.00 $350.00 $578.00 | ||
7-epi-Taxol exhibits remarkable properties as an antineoplastic agent through its ability to stabilize microtubules, disrupting normal mitotic processes. This stabilization prevents the depolymerization of tubulin, leading to cell cycle arrest. Its unique stereochemistry enhances binding affinity to the β-tubulin subunit, promoting altered dynamics in cellular architecture. Additionally, 7-epi-Taxol's hydrophobic characteristics facilitate interactions with lipid membranes, influencing cellular signaling pathways. | ||||||
Amrubicin | 110267-81-7 | sc-207289 | 5 mg | $1051.00 | 3 | |
Amrubicin is a synthetic anthracycline that intercalates into DNA, disrupting the replication process by inhibiting topoisomerase II. This interaction leads to the formation of DNA double-strand breaks, triggering cellular apoptosis. Its unique planar structure allows for effective stacking between base pairs, enhancing its binding affinity. Furthermore, Amrubicin's lipophilic nature aids in membrane permeability, influencing cellular uptake and distribution, which can affect its overall efficacy in cellular environments. | ||||||
Raltitrexed | 112887-68-0 | sc-219933 | 10 mg | $146.00 | ||
Raltitrexed is a potent antineoplastic agent that acts as a thymidylate synthase inhibitor, disrupting the de novo synthesis of thymidine. Its unique structure allows for tight binding to the enzyme's active site, effectively blocking the conversion of deoxyuridine monophosphate to thymidine monophosphate. This inhibition leads to a depletion of thymidine, ultimately impairing DNA synthesis and repair. Raltitrexed's selective targeting of rapidly dividing cells highlights its specificity in disrupting cellular proliferation pathways. | ||||||