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RG3039(PF-06687859)

  Cat. No.:  DC7551   Featured
Chemical Structure
1005504-62-0
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More than 5000 active chemicals with high quality for research!
Field of application
For the detailed information of PF-0668759, the solubility of PF-0668759 in water, the solubility of PF-0668759 in DMSO, the solubility of PF-0668759 in PBS buffer, the animal experiment (test) of PF-0668759, the cell expriment (test) of PF-0668759, the
Chemicals PropertiesBiological activity COA & MSDSRelated productsDatasheet
Cas No.: 1005504-62-0
SMILES: NC1=NC(N)=C2C(OCC3CCN(CC4=C(Cl)C=CC=C4Cl)CC3)=CC=CC2=N1
Formula: C21H23Cl2N5O
M.Wt: 432.346222162247
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: RG3039 (PF-06687859) is an orally bioavailable and brain-penetrant DcpS inhibitor with an IC50 of 0.069 nM.
In Vivo: RG3039 can extend survival and improve function in two SMA mouse models of varying disease severity (Taiwanese 5058 Hemi and 2B/− SMA mice), and positively impacts neuromuscular pathologies. In 2B/− SMA mice, RG3039 provides a >600% survival benefit (median 18 days to >112 days) when dosing began at P4, highlighting the importance of early intervention[2]. RG3039 distributes to central nervous system tissues where it robustly inhibits DcpS enzyme activity, but minimally activates SMN expression or the assembly of small nuclear ribonucleoproteins. RG3039 treated SMA mice shows a dose-dependent increase in survival, weight and motor function and it is associated with improved motor neuron somal and neuromuscular junction synaptic innervation and function and increased muscle size. RG3039 also enhances survival of conditional SMA mice in which SMN has been genetically restored to motor neurons[3].
In Vitro: RG3039 is a dibasic lipophilic molecule that is predicted to accumulate in lysosomes[1]. In motor neurons, RG3039 significantly increases both the average number of cells with gems and average number of gems per cell, which is used as an indirect measure of SMN levels[2].
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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