HO-PEG15-OH is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
Amino-PEG15-amine is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
Azido-PEG15-azide is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
Azido-PEG15-t-butyl ester is a polyethylene glycol (PEG) derived linker, specifically designed for the synthesis of proteolysis-targeting chimeras (PROTACs)[1].
Bis-PEG15-acid is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
Boc-NH-PEG15-azide is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
Boc-NH-PEG15-NH2 is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
Cbz-N-PEG15-amine is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
m-PEG15-alcohol is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
m-PEG15-NHS ester is a PEG-based linker for PROTACs which joins two essential ligands, crucial for forming PROTAC molecules. This linker enables selective protein degradation by leveraging the ubiquitin-proteasome system within cells.
ARRY-403, also known as AMG-151, is an orally available allosteric glucokinase (GK) activator developed for the treatment of type 2 diabetes mellitus (T2DM). ARRY-403 has many favorable physicochemical characteristics and ADME properties (low potential to cause drug–drug interactions (DDIs). ARRY-403 potently activates human glucokinase (GK) in vitro (EC50 = 79 nM at 5 mM glucose), with an S0.5 = 0.93 mM glucose (ARRY-403 at 5 mM) and Vmax = 134% compared to the no activator control. It possesses good in vitro drug-like properties (aqueous solubility, cell permeability, low low potential for drug-drug interactions, low predicted hepatic clearance), and selectivity against broad panels of receptors and enzymes.
PD153035 is a ATP-competitive EGFR inhibitor with an IC50 and Ki of 25 and 6 pM. PD153035 effectively blocks the enhancement of mitogenesis, induction of early gene expression, and oncogenic transformation that occur in response to EGF receptor stimulation. With human fibroblasts and epidermoid carcinoma cells, PD153035 at nanomolar concentrations rapidly inhibits EGFR autophosphorylation. With breast and ovarian cancer cells, PD153035 not only blocks cell growth via inhibition of EGFR, but also upregulates the expression of the tumor suppressor retinoic acid receptor-beta 2 (RAR-beta2).
YM-543, also known as ASP-543, is a selective SGLT2 inhibitor. Sodium-glucose cotransporter 2 (SGLT2) is a specifically expressed transporter in the kidney that plays an important role in renal glucose reabsorption, and its inhibition may present a novel therapeutic strategy for treating diabetes. YM543 potently and selectively inhibited mouse and human SGLT2 activities at nanomolar ranges. In vivo single oral administration of YM543 dose-dependently and significantly reduced blood glucose levels and improved glucose tolerance with a concomitant increase in urinary glucose excretion in KK Ay type 2 diabetic mice, effects that were sustained even after 12 h.