Life Science

A 2&#39 deoxy analog of 5-azacytidine which is incorporated into DNA and causes hypomethylation by inhibiting DNA methyltransferases in a concentration-dependent manner useful in conditions characterized by DNA hypermethylation, as is found in

A 2&#39 deoxy analog of 5-azacytidine which is incorporated into DNA and causes hypomethylation by inhibiting DNA methyltransferases in a concentration-dependent manner useful in conditions characterized by DNA hypermethylation, as is found in

A 2&#39 deoxy analog of 5-azacytidine which is incorporated into DNA and causes hypomethylation by inhibiting DNA methyltransferases in a concentration-dependent manner useful in conditions characterized by DNA hypermethylation, as is found in

Cas No : 58846-77-8 MDL No : MFCD00063297 MolecularFormula : C16H32O6 MolecularFormula : C16H32O6 Molecular Weight : 320.42 Purity Limit : &gt 97% Storage Temp : Store at 0-8 &degC Appearance : White Powder

Cas No : 58846-77-8 MDL No : MFCD00063297 MolecularFormula : C16H32O6 MolecularFormula : C16H32O6 Molecular Weight : 320.42 Purity Limit : &gt 97% Storage Temp : Store at 0-8 &degC Appearance : White Powder

A dose-dependent inhibitor of FAK, with maximal inhibition of FAK autophosphorylation in cells achieved at 10 &microM restores the chemosensitivity of taxane-resistant cells to paclitaxel orally bioavailable, inhibiting FAK and augmenting

A dose-dependent inhibitor of FAK, with maximal inhibition of FAK autophosphorylation in cells achieved at 10 &microM restores the chemosensitivity of taxane-resistant cells to paclitaxel orally bioavailable, inhibiting FAK and augmenting

A dose-dependent inhibitor of FAK, with maximal inhibition of FAK autophosphorylation in cells achieved at 10 &microM restores the chemosensitivity of taxane-resistant cells to paclitaxel orally bioavailable, inhibiting FAK and augmenting

A dose-dependent inhibitor of FAK, with maximal inhibition of FAK autophosphorylation in cells achieved at 10 &microM restores the chemosensitivity of taxane-resistant cells to paclitaxel orally bioavailable, inhibiting FAK and augmenting

A synthetic, tridentate iron-selective chelator that dramatically reduces iron in the liver and blood, particularly during transfusional iron overload orally bioavailable, effectively reducing liver, serum, and cardiac iron concentration in

A synthetic, tridentate iron-selective chelator that dramatically reduces iron in the liver and blood, particularly during transfusional iron overload orally bioavailable, effectively reducing liver, serum, and cardiac iron concentration in

A synthetic, tridentate iron-selective chelator that dramatically reduces iron in the liver and blood, particularly during transfusional iron overload orally bioavailable, effectively reducing liver, serum, and cardiac iron concentration in