The high valent molybdenum-dioxo complex MoO2Cl2 catalyzes the addition of dimethylphenylsilane to aldehydes and ketones to afford the corresponding dimethylphenylsilyl ethers in quantitative yield.
The molybdenum(II) tricarbonyl complexes Mo(CO)
3
I
2
L
n
(
n
= 1, L = 2,2′-bipyridine, 4,4′-di-
tert
-butyl-2,2′-bipyridine;
n
= 2, L = pyridine, 4-
tert
-butylpyridine) have been examined as ...catalyst precursors for the epoxidation of the biorenewable olefin methyl oleate with
tert
-butylhydroperoxide. In situ oxidative decarbonylation of the precursors gives highly active and selective molybdenum(VI) catalysts, which were identified as the one-dimensional molybdenum oxide/bipyridine polymer MoO
3
(2,2′-bipyridine), octanuclear Mo
8
O
24
(4,4′-di-
tert
-butyl-2,2′-bipyridine)
4
, and the pyridinium β-octamolybdates (LH)
4
Mo
8
O
26
for L = pyridine or 4-
tert
-butylpyridine.
Graphical Abstract
Complexes of the general formula MoO2X2L2 (X=Cl, Br, Me; L2=bipy, bpym) have been prepared and fully characterized, including X‐ray crystallographic investigations of all six compounds. Additionally, ...the highly soluble complex MoO2Cl2(4,4′‐bis(hexyl)‐2,2′‐bipyridine) has been synthesized. The reaction of the complexes with tert‐butyl hydroperoxide (TBHP) is an equilibrium reaction, and leads to MoVI η1‐alkylperoxo complexes that selectively catalyze the epoxidation of olefins. Neither the Mo−X bonds nor the Mo−N bonds are cleaved during this reaction. These experimental results are supported by theoretical calculations, which show that the attack of TBHP at the Mo center through the X‐O‐N face is energetically favored and the TBHP hydrogen atom is transferred to a terminal oxygen of the Mo=O moiety. After the attack of the olefin on the Mo‐bound peroxo oxygen atom, epoxide and tert‐butyl alcohol are formed. The latter compound acts as a competitive inhibitor for the TBHP attack, and leads to a significant reduction in the catalytic activity with increasing reaction time.
Complexes of the general formula MoO2X2L2 with (X = Cl, Br, Me and L2 = bipy, bpym; an example is illustrated here) have been prepared, fully characterized (including X‐ray crystallography), and their catalytic performance in olefin epoxidation was investigated. Furthermore, the highly soluble complex MoO2Cl2(4,4′‐bis(hexyl)‐2,2′‐bipyridine) has been synthesized, which allowed mechanistic studies to be undertaken. The experiments show the formation of a η1‐alkylperoxo species; the results are supported by theoretical calculations.
The indenyl molybdenum carbonyl complexes IndMo(CO)2(L)nBF4 (L = NCMe with n = 3 (1), 2,2′-bipyridine (2) or 1,4,7-trimethyltriazacyclononane (3) with n = 1) promote epoxide alcoholysis under ...moderate reaction conditions. Complexes 1 and 2 showed the best performance for the alcoholysis of styrene oxide with different alcohol nucleophiles (acting as both reactant and solvent), leading to the corresponding 2-alkoxy-2-phenylethanol with 100% yield at 10 min and 35 °C. These catalytic results are far superior to those found for previously studied molybdenum carbonyl complexes. An efficient procedure for catalyst recovery and reuse without decrease in reaction rate is described.
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•Cationic IndMo(CO)2(L)n+ complexes as (pre)catalysts for styrene oxide alcoholysis.•MeOH, EtOH or BuOH as solvent and reactant to give 2-alkoxy-2-phenylethanol (APE).•Quantitative yield of APE within 1 min at 35 °C and 5 mol% (pre)catalyst.•Catalytic performance surpasses that of previously studied Mo carbonyl complexes.•Recycling of homogeneous catalyst/ionic-liquid system with retention of performance.
We demonstrate that RuII(CO)2–protein complexes, formed by the reaction of the hydrolytic decomposition products of fac‐RuCl(κ2‐H2NCH2CO2)(CO)3 (CORM‐3) with histidine residues exposed on the surface ...of proteins, spontaneously release CO in aqueous solution, cells, and mice. CO release was detected by mass spectrometry (MS) and confocal microscopy using a CO‐responsive turn‐on fluorescent probe. These findings support our hypothesis that plasma proteins act as CO carriers after in vivo administration of CORM‐3. CO released from a synthetic bovine serum albumin (BSA)–RuII(CO)2 complex leads to downregulation of the cytokines interleukin (IL)‐6, IL‐10, and tumor necrosis factor (TNF)‐α in cancer cells. Finally, administration of BSA–RuII(CO)2 in mice bearing a colon carcinoma tumor results in enhanced CO accumulation at the tumor. Our data suggest the use of RuII(CO)2–protein complexes as viable alternatives for the safe and spatially controlled delivery of therapeutic CO in vivo.
Artificial metalloproteins release carbon monoxide spontaneously in aqueous solution, cells, and mice. The RuII(CO)2–protein complexes were formed from the reaction of the hydrolytic decomposition products of CO‐releasing molecule 3 (CORM‐3) with histidine residues exposed on the surface of proteins.
The synthesis and characterization of new ring-functionalized molybdenocene derivatives CpCp′Mo(CO)22+ and CpCp′Mo(CO)Br+ (η5-C5H4R; R = CH2CH2OMe, CH2CH2COOEt, CH2CH2OOCMe, COOMe) are reported. ...Three alternative routes were used to assemble the CpCp′Mo moiety. Following route I, the unsubstituted precursor CpMo(CO)2(NCMe)2+ reacts with substituted cyclopentadienes (Cp′H) to give after oxidation dicationic compounds CpCp′Mo(CO)22+. Alternatively, route II introduces the substituent in the first reaction step upon the synthesis of Cp′Mo(CO)2(NCMe)2+. In this case, the bis-cyclopentadienyl compounds CpCp′Mo(CO)22+ were obtained after reaction with cyclopentadiene (C5H6) and subsequent oxidation. The NMR spectroscopic measurements prove that the reaction pathways of routes I and II go through different intermediates. The bromo complexes CpCp′Mo(CO)Br+ were synthesized using route III. Reaction of Cp′Mo(CO)2(NCMe)2+ with C5H5SiMe3 gives hydride complexes CpCp′Mo(CO)H+. Appropriate bromo complexes were obtained upon reaction with bromine. The ring-functionalized bis-cyclopentadienyl molybdenum(IV) compounds and their monocyclopentadienyl precursors were characterized by spectroscopic methods. Structures of CpMo(η5-C5H4CH2CH2COOEt)(CO)2MoOBr4(H2O)Br, (η5-C5H4COOMe)Mo(η3-C3H5)(CO)2, (η5-C5H4COOMe)Mo(CO)2(NCMe)2BF4, (η5-C5H4SiMe3)Mo(CO)2(NCMe)2BF4, and CpMo(η5-C5H4COOMe)(CO)HBF4 were determined with X-ray diffraction analysis.
Romao et all discuss the synthetic, structural, spectroscopic, and other relevant studies of the inorganic and organometallic Re(VII) oxides. Much more research in this area needs to be done.
The toxicity profile of
fac
-Re(CO)
3
(N-N)L
+
complexes against microbial and tumoral cells has been extensively studied, primarily focusing on modifications to the bidentate diimine (N-N) ligand. ...However, less attention has been paid to modifications of the axial ligand L, which is perpendicular to the Re-N-N plane. This study reveals that the high toxicity of the
fac
-Re(CO)
3
(bpy)(Ctz)
+
complex may be attributed to the structural effect of the trityl (CPh
3
) group present in clotrimazole, as removal of phenyl rings causes a significant decrease in the activity against
Staphylococcus aureus
(
S. aureus
). Moreover, substitution of the 1-tritylimidazole ligand by the structurally related ligands PPh
3
and PCy
3
maintains similarly high activity levels. These findings contribute to understanding the interactions of toxic complexes with bacterial membranes, suggesting that the ligand structures play a crucial role in inhibiting cell wall synthesis processes, potentially including Lipid II synthesis. Compounds with Ph
3
E (E = C-imidazole; P) groups also showed to be 10 times more toxic than cisplatin against three mammalian cell lines (IC
50
: 2-4 μM). In contrast, the analogue 1-benzylimidazole and 1-
tert
-butylimidazole derivatives were as toxic as cisplatin. We observed that the decomposition of the Re
(I)
(CO)
3
fragment inside mammalian cell lines liberates CO, which is expected to exert biological effects. Therefore, compounds of this family possessing the structural motif Ph
3
E seem to combine high antimicrobial and antitumoral activities, the latter being much higher than that of cisplatin.
The bulky pyramidal structures of CPh
3
and PPh
3
impart high antimicrobial and anti-tumoral activities to the Re(CO)
3
bpy
+
moiety.
The toxicity profile of fac-Re(CO)3(N-N)L+ complexes against microbial and tumoral cells has been extensively studied, primarily focusing on modifications to the bidentate diimine (N-N) ligand. ...However, less attention has been paid to modifications of the axial ligand L, which is perpendicular to the Re-N-N plane. This study reveals that the high toxicity of the fac-Re(CO)3(bpy)(Ctz)+ complex may be attributed to the structural effect of the trityl (CPh3) group present in clotrimazole, as removal of phenyl rings causes a significant decrease in the activity against Staphylococcus aureus (S. aureus). Moreover, substitution of the 1-tritylimidazole ligand by the structurally related ligands PPh3 and PCy3 maintains similarly high activity levels. These findings contribute to understanding the interactions of toxic complexes with bacterial membranes, suggesting that the ligand structures play a crucial role in inhibiting cell wall synthesis processes, potentially including Lipid II synthesis. Compounds with Ph3E (E = C-imidazole; P) groups also showed to be 10 times more toxic than cisplatin against three mammalian cell lines (IC50: 2-4 μM). In contrast, the analogue 1-benzylimidazole and 1-tert-butylimidazole derivatives were as toxic as cisplatin. We observed that the decomposition of the Re(I)(CO)3 fragment inside mammalian cell lines liberates CO, which is expected to exert biological effects. Therefore, compounds of this family possessing the structural motif Ph3E seem to combine high antimicrobial and antitumoral activities, the latter being much higher than that of cisplatin.The toxicity profile of fac-Re(CO)3(N-N)L+ complexes against microbial and tumoral cells has been extensively studied, primarily focusing on modifications to the bidentate diimine (N-N) ligand. However, less attention has been paid to modifications of the axial ligand L, which is perpendicular to the Re-N-N plane. This study reveals that the high toxicity of the fac-Re(CO)3(bpy)(Ctz)+ complex may be attributed to the structural effect of the trityl (CPh3) group present in clotrimazole, as removal of phenyl rings causes a significant decrease in the activity against Staphylococcus aureus (S. aureus). Moreover, substitution of the 1-tritylimidazole ligand by the structurally related ligands PPh3 and PCy3 maintains similarly high activity levels. These findings contribute to understanding the interactions of toxic complexes with bacterial membranes, suggesting that the ligand structures play a crucial role in inhibiting cell wall synthesis processes, potentially including Lipid II synthesis. Compounds with Ph3E (E = C-imidazole; P) groups also showed to be 10 times more toxic than cisplatin against three mammalian cell lines (IC50: 2-4 μM). In contrast, the analogue 1-benzylimidazole and 1-tert-butylimidazole derivatives were as toxic as cisplatin. We observed that the decomposition of the Re(I)(CO)3 fragment inside mammalian cell lines liberates CO, which is expected to exert biological effects. Therefore, compounds of this family possessing the structural motif Ph3E seem to combine high antimicrobial and antitumoral activities, the latter being much higher than that of cisplatin.
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