MuseChem is a leading supplier of custom peptide synthesis services. With rich knowledge and expertise in peptide synthesis and proprietary platform technologies, we offer a wide range of peptide synthesis services from bulk API peptides production to complex peptide modifications. We have an experienced team of scientists who are able to choose and optimize the appropriate peptide synthesis method for each peptide, so our peptide synthesis service has a very high success rate. Each peptide comes with a complete quality control package, which includes HPLC and MS Analysis.
Features of our custom peptide synthesis
● Free peptide design and consultation
● Custom synthesis of peptide, peptides building blocks and peptide fragments
● Small scale high throughput peptide library synthesis to bulk quantity peptides production
● Solid and solution phase synthesis
● Recombinant peptide technology for producing long peptide (>200 amino acids)
● State-of-the-art analytical support (LCMS, HPLC, AA analyzer)
Custom synthesis of modified peptides
MuseChem also has a strong capability in supplying a variety of modified peptides, include, not limited to:
● Isotope labeled peptides
● Fluorescent & FRET peptides
● Cyclic peptides
● Stapled peptides
● Amidated peptides
● Acetylated peptides
● Biotinylated peptides
● Citrullinated peptides
● Phosphorylated peptides
● PEGylated peptides
SB1317(TG-02) is a novel small molecule potent CDK2/JAK2/FLT3 inhibitor with IC50s of 13/73/56 nM respectively. TG02 is a novel pyrimidine-based multi-kinase inhibitor that inhibits CDKs 1, 2, 7 and 9 together with JAK2 and FLT3. It dose-dependently inhibits signaling pathways downstream of CDKs, JAK2 and FLT3 in cancer cells with the main targets being CDKs. TG02 is anti-proliferative in a broad range of tumor cell lines, inducing G1 cell cycle arrest and apoptosis. In vivo, TG02 exhibits favorable pharmacokinetics after oral dosing in xenograft models and accumulates in tumor tissues, inducing an effective blockade of both CDK and STAT signaling. TG02 induces tumor regression after oral dosing on both daily and intermittent schedules in a murine model of mutant-FLT3 leukemia (MV4-11) and prolongs survival in a disseminated AML model with wild-type FLT3 and JAK2 (HL-60). TG02 is active in various models of leukemia and provide a rationale for the ongoing clinical evaluation of TG02 i...
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