1.17.4.2	2',2'-difluoro-2'-deoxycytidine 5'-triphosphate	complete inactivation of the enzyme by 1 equiv of 2',2'-difluoro-2'-deoxyCTP, F2CTP, in about 2 min proceeding via alkylation by the sugar of F2CTP and AdoCbl destruction. 0.47 equiv of a sugar moiety is covalently bound to RNR and 0.25 equiv of a cobalt(III) corrin is tightly associated, likely through a covalent interaction with C419 (Co-S) in the active site of RNR. Analysis of the relationship of the nonalkylative pathway for RNR inactivation relative to the alkylative pathway, overview	85040	
1.17.4.2	2',2'-difluoro-2'-deoxycytidine 5'-triphosphate	F2CTP, a clinically used anti-cancer drug, synthesis, overview. Causes rapid enzyme inactivation through covalent modification, mechanism of inactivation, analysis by mass spectrometry and radio- or deuterium-labeled compounds, overview. C119 is involved in the reaction	85040	
1.17.4.2	2'-chloro-2'-deoxy-UTP	-	165857	
1.17.4.2	2'-deoxyadenosylcobalamin	-	107951	
1.17.4.2	3,3',4,4',5,5'-hexahydroxy-trans-stilbene	i.e. M8, a resveratrol analogue, inhibits the enzyme and causes an imbalance of intracellular dNTP pools, the dATP pool is eliminated, while the dCTP and dTTP pools are enlarged. M8 leads to complete growth inhibition of HT-29 cells at 0.015 mM within 7 days, overview	143587	
1.17.4.2	3-aminopyridine-2-carboxaldehyde thiosemicarbazone	i.e.3-AP or triapine, in combination with the nucleoside analog fludarabine for patients with refractory acute leukemias and aggressive myeloprol, phase I study, detailed overview, the inhibitor inhibits the M2 subunit, and depletes intracellular deoxyribonculeotide pools, especially dATP	37696	
1.17.4.2	3-aminopyridine-2-carboxaldehyde-thiosemicarbazone	i.e. 3-AP, phase I study in combination with high dose cytarabine in patients with advanced myeloid leukemia, resulting in enhanced cytarabine cytotoxicity with possible methemoglobinemia, overview	68825	
1.17.4.2	3-isoadenosylcobalamin	-	108312	
1.17.4.2	adenosylcobalamin	-	578	
1.17.4.2	caracemide	-	10338