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 Diaryliodonium salts are well-known to transfer an aryl group to carbon and heteroatom nucleophiles, and in some cases a base is required [1]. However, transition metal catalysts and supporting ligands are not needed. Moreover, reactions conducted with diaryliodonium salts are operationally simple because they are non-toxic and are not sensitive to air or moisture. Therefore diaryliodonium salts offer an important alternative to metal-catalyzed arylation reactions. Despite these attractive characteristics, a major obstacle to their adoption in chemical synthesis and discovery chemistry has been commercial availability.
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 It is proved that a diverse compound library is the most successful and straightforward starting point to find new leads. Moreover, it is the best way to enhance your research compound collections by adding new substances with different chemotypes.
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The OTAVA G9a Targeted Library comprises 561 carefully curated small molecules aimed at modulating the activity of histone methyltransferase G9a (EHMT2)—a master regulator of transcriptional repression through histone H3 lysine 9 (H3K9) methylation. This collection provides a powerful resource for researchers exploring epigenetics-driven mechanisms in cancer, neurodegeneration, inflammation, and stem cell reprogramming.
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 Our Halogen-Enriched Fragment Library comprises 708 brominated fragments that can explore binding sites for favorable halogen bond interactions to identify unique binding modes that are complementary to those obtained from classical fragment-based screening.
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Histone deacetylase 1 (HDAC1; also known as GON-10, RPD3, or KDAC1) is a key epigenetic regulator involved in chromatin remodeling and gene expression. Aberrant HDAC1 activity has been implicated in tumorigenesis, and it is widely recognized as a high-value target for cancer therapy due to its role in promoting oncogenic transcriptional programs.
The mechanistic target of rapamycin (mTOR; also referred to as FRAP1, RAFT1, or RAPT1) is a central serine/threonine kinase that integrates nutrient and growth factor signals to regulate cell growth, proliferation, metabolism, and autophagy. Hyperactivation of mTOR signaling is a hallmark of various malignancies, contributing to uncontrolled tumor cell survival and resistance to therapy.
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