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Sulfanilamide
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Nine patients allergic to sulfanilamide were patch tested with a battery of 25 sulfonamides (all tested 5% pet.) to detect cross-sensitization and there were 3 reactions to sodium sulfadiazine, 2 to sodium sulfacetamide, one to sulfaguanidine, one to sodium sulfadimidine and one to sodium sulfamerazine (6).
M
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Marshall, Eli Kinnerly (1889–1966) American pharmacologist and physiologist at the Johns Hopkins in Baltimore. He demonstrated the secretory function of the renal convoluted tubule by using phenolsulfonephthalein in 1924. He introduced sulfaguanidine for treatment of bacillary dysentery in 1941.
Sulfonamides
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Natasha E. Holmes, M. Lindsay Grayson
Both the nonabsorbed sulfonamides, such as sulfaguanidine, and the well-absorbed short-acting sulfonamides (e.g. sulfadiazine or sulfadimidine) have been used extensively in the past for treatment of shigella dysentery. These drugs are now rarely useful alone for this disease as a result of increasing sulfonamide resistance. Resistance to cotrimoxazole, one of the earlier drugs of choice in the treatment of shigellosis, is now common among Shigella dysenteriae type 1 strains in Africa and Asia and is increasing in other Shigella species, including S. sonnei, in the USA and elsewhere (Salam and Bennish, 1991; see Chapter 92, Trimethoprim and trimethoprim–sulfamethoxazole [cotrimoxazole]). Sulfonamides have never been useful for the treatment of salmonellosis.
6-(2-Morpholinoethyl)-thiazolo[3,2-a]pyrimidin-5-one: A novel scaffold for the synthesis of potential PI3kα inhibitors
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Ahmed R. Ali, Eman R. El-Bendary, Mariam A. Ghaly, Ihsan A. Shehata
In light of the NCI results, the following could be considered: Regarding the sensitivity against individual cell lines in Table 1, all target compounds 4–6(a–c) showed observed low cell growth promotion against Renal UO-31cancer cell line with cell growth promotion varying from 52.72% to 64.52%.By comparing the results from different series, it was found that the introduction of sulfacetamide in compounds 5a–c or sulfaguanidine in compounds 6a–c instead of morpholine moiety in compounds 4a–c proved to enhance the potency towards Renal UO-31cancer cell line and reduce potency towards Leukemia SR cancer cell line.It is worth mentioning that compounds 4–6(a) exhibited increased potency towards Leukemia SR cancer cell line and reduced the potency towards Non-Small Cell Lung HOP-92 cancer.
Effect of hydrophobic extension of aryl enaminones and pyrazole-linked compounds combined with sulphonamide, sulfaguanidine, or carboxylic acid functionalities on carbonic anhydrase inhibitory potency and selectivity
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Heba Abdelrasheed Allam, Mohamed E. Albakry, Walaa R. Mahmoud, Alessandro Bonardi, Shaimaa A. Moussa, Samy Mohamady, Hatem A. Abdel-Aziz, Claudiu T. Supuran, Hany S. Ibrahim
The ubiquitous and physiologically predominant isoform hCA II was significantly inhibited by the enaminone-sulphonamide analogues 3a–3c with inhibition constants between 49.6 and 65.3 nM. The replacement of sulphonamide by sulfaguanidine group as in analogues 3d–3f, significantly reduced the activity with inhibition constants between 607.9 and 822.3 nM while replacement with COOH as in analogues 5a–5c completely abolished the activity. The heterocycloalkyl substituents in compounds 4a–4c exhibited moderate inhibitory activity with inhibition constants between 586.7 and 689.2 nM probably due to unfavourable steric clashes.
2-((1H-Benzo[d]imidazol-2-yl)amino)benzo[d]thiazole-6-sulphonamides: a class of carbonic anhydrase II and VII-selective inhibitors
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Morteza Abdoli, Claudiu T. Supuran, Raivis Žalubovskis
The following structure activity relationship (SAR) can be figured out from the inhibition data of Table 1:Among the entire series, only compounds bearing primary sulphonamide moiety 6a–c and 7a–c were moderately inhibited the cytosolic isoform hCA I, whereas sulphaguanidine derivatives 9a–d were entirely inactive against this isoform (KI > 100 µM). The SAR showed that compounds containing imidazoline core 6a–c displayed better inhibitory capability against this isoform, with KIs ranging between 442.4 and 7590 nM, as compared to the benzimidazoline-substituted ones 7a–c (KIs of 4927–9533 nM). Notably, the inhibitory potency was reduced significantly when any functionality was presented on the periphery of(benz)imidazoline rings. As shown in Table 1, 2-((4,5-dihydro-imidazol-2-yl)amino)benzothiazole-6-sulphonamide 6a exhibited the best activity of all the evaluated compounds, albeit approximately two-fold less effective than standard drug, AAZ.The physiologically most relevant isoform hCA II was inhibited by compounds 6a–c and 7a–c more than hCA I (KIs in the range 37.6–577.6 nM). The results showed that sulphaguanidines 9a–d were also inactive against this isoform. Again imidazoline-incorporated sulphonamides 6a–c demonstrated superior inhibitory activities (KIs in the range 37.6–65.6 nM) compared to benzimidazoline-substituted derivatives 7a–c (KIs of 84.0–577.6 nM). Once more, the optimal substitution seems to be an unsubstituted imidazoline ring, in 6a, which is the most effective hCA II inhibitor in the series investigated here.As seen from data of Table 1, none of the tested compounds showed inhibitory action against the transmembrane isoform hCA IV (KI > 100 µM), which is considered as being an off-target isoform in our study. Notably, AAZ shows low nanomolar inhibitory activity against this isoform with a KI of 74nM.Similar to the inhibitory pattern of investigated compounds against ubiquitous CA I and CA II, sulphaguanidine derivatives 9a–d failed to inhibit the neuropathic pain associated hCA VII. However, the rest of the derivatives 6a–c and 7a–c effectively inhibited this isoform, with KIs values ranging from 37.4to 694.4 nM. Although again analogues 6a–c exhibited better inhibitory activity when compared to compounds 7a–c, in this case, the SAR was not very flat. Indeed, compound 6a has the highest inhibitory effect for the off-target isoforms hCA I and hCA II while methyl-substituted compound 6b showed superior inhibitory potency towards hCA VII. Although this compound displayed 15-fold higher selectivity for hCA VII over hCA I, it did not show significant selectivity towards hCA VII versus hCA II (hCA VII/hCA II ≈ 1.3).