|Catalog||Product Name||CAS Number|
|It is produced by the strain of Amanita phalloides. It is highly toxic to humans and can cause salivation, vomiting, bleeding, diarrhea, cyanosis, muscle convulsions, spasms, and death. Used as a rese...|
|MC-Val-Cit-PAB-rifabutin is a drug-linker conjugate for ADC with potent antitumor activity by using rifabutin (an DNA-dependent RNA polymerase inhibitor), linked via the ADC linker MC-Val-Cit-PAB.|
|MC-VC-PABC-DNA31 is a drug-linker conjugate for ADC with potent antitumor activity by using DNA31 (a potent RNA polymerase inhibitor), linked via the ADC linker MC-VC-PABC.|
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RNA polymerase (RNAP) is an enzyme that synthesizes RNA using a DNA strand or RNA as a template, ribonucleoside triphosphate as a substrate, and polymerizes through a phosphate diester bond. Three RNA polymerases carry out eukaryotic gene transcription: RNA polymerase I (Pol I), RNA polymerase II (Pol II) and RNA polymerase III (Pol III). The majority of regulatory activities (such as binding of gene-specific transcription factors and chromatin-remodeling activities) ultimately result in the modulation of RNA polymerase activities by controlling its initiation, elongation, and termination properties. A comprehensive understanding of the mechanisms operating within RNAP and how these mechanisms are modified at the various stages of the transcription cycle are the most critical challenges in biomedicine currently.
During the past decades, the primary focus has been on RNA Pol II in malignancy. However, the ‘odd’ RNA Pols: RNA Pol I and RNA Pol III are not idle bystanders in cancer etiology. Even though the range of target genes of RNA Pol I and RNA Pol III transcribe is considerably smaller than RNA Pol II, their non-coding RNA transcripts account for over 50% of all transcription in actively growing cells. Their dysregulated expression is a consistent feature of tumor cells. In the case of RNA Pol I, its overactivity is necessary for hematological tumor cells' survival and can be therapeutically targeted in vivo. Moreover, a demonstration revealed RNA Pol II‑dependent sequence-specific transcription factors can directly interact with and modulate the core RNA Pol I and RNA Pol III transcription apparatus in most cancer settings. This observation suggests that hijacking the control of RNA Pols might be essential for malignant transformation. Indeed, the most effective and common carcinogenic and tumor suppressor components in the transcription apparatus seem to regulate all three RNA Pols. Cancer genome-sequencing projects have recently revealed that mutations occur in a broader range of RNA Pol transcriptional apparatus components than previously thought. These include co‑repressors, co‑activators, components of the mediator complex, chromatin modifiers, and even factors involved in RNA Pol transcription elongation.
Components of the core transcription apparatus, including the mediator complex and the SEC, represent bone fide therapeutic targets for cancer treatment not only as advanced broad-spectrum cytotoxins but also as part of the novel paradigm for personalized medicine. The potential therapeutic benefit of selectively inhibiting the RNA polymerase target to cancer cell survival prompted the need to identify small molecule drugs that selectively inhibit RNA synthesis. Indeed, there have been numerous clinically approved cytotoxic drugs whose therapeutic effect is associated with the disruption of ribosome biogenesis.