Gentamicin Sulfate

Gentamicin Sulfate

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Gentamicin Sulfate
Category Antibiotics
Catalog number BBF-05841
CAS 1405-41-0
Molecular Weight 561.65 (Average)
Molecular Formula C(19-21)H(39-43)N5O7.H2SO4
Purity Assay: ≥ 590 I.U./mg

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BBF-05841 50 g $299 In stock

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Description

Gentamycin Sulfate is a broad-spectrum, aminoglycoside antibiotic used for cell culture which inhibits protein synthesis in sensitive organisms.

Specification

Synonyms Gentamicin C; NSC-82261; NSC82261; NSC 82261; SCH9724; SCH 9724; SCH-9724; Alcomicin; Bristagen; Cidomycin; Duragentam; Garamycin; Garasol; Genoptic; Gentacidin; Gentacin; Gentaglyde; Gentalyn; Gentamicin C Complex Citrate; Gentibioptal; Genticin; Gentocin; Gentogram; Gent-Ophtal; Getalline; GM Sulfate
Storage Store at -20°C

Properties

Appearance White to Off-white Solid
Application broad-spectrum, aminoglycoside antibiotic
Antibiotic Activity Spectrum Gram-positive bacteria; Gram-negative bacteria; Mycoplasma
Boiling Point 797.6°C at 760 mmHg
Melting Point 218-237°C
Solubility Soluble in Water (Slightly)

Reference Reading

1.Collagen implant with gentamicin sulphate as an option to treat a neuroischaemic diabetic foot ulcer: Case report.
Costa Almeida CE1. Int J Surg Case Rep. 2016 Feb 26;21:48-51. doi: 10.1016/j.ijscr.2016.02.023. [Epub ahead of print]
INTRODUCTION: The ischaemic diabetic foot is associated with a faster evolving atherosclerosis affecting preferentially the bellow knee arteries. This distal ischemia associated with a wide distribution of multiple stenosis and occlusions throughout lower limb arteries, makes revascularization very hard or even impossible. This represents a major factor responsible for non-healing diabetic foot ulcer. In these cases all efforts should be made to find treatment alternatives that can promote ulcer healing.
2.Protective Effect of Ginkgo Biloba Extract on Gentamicin-Induced Structural Changes of Calcite-Gelatin Composite.
Jang CH1, Cho YB, Lee JK. J Int Adv Otol. 2015 Dec;11(3):179-82. doi: 10.5152/iao.2015.1605.
OBJECTIVE: To evaluate the protective effect of Ginkgo biloba extract (GBE) on gentamicin (GM)-induced morphological damage of an artificial otoconia.
3.A rapid and sensitive method for kinetic study and activity assay of DNase I in vitro based on a GO-quenched hairpin probe.
Xu W1, Xie Z1, Tong C2, Peng L1, Xiao C1, Liu X1, Zhu Y1, Liu B3. Anal Bioanal Chem. 2016 Apr 1. [Epub ahead of print]
As a waste-management endonuclease, DNase I has been suggested to be one of the deoxyribonucleases responsible for DNA fragmentation during apoptosis. We report here an alternative fluorescence method for DNase I assay with high accuracy and sensitivity by applying a DNA/GO (graphene oxide) probe. The method with a detection limit of 1 U mL-1 was then applied to investigate the effects of external factors including antibiotics and heavy metal ions on DNase I. The results demonstrated that gentamicin sulfate was a strong inhibitor with an IC50 value of 0.57 ± 0.12 mM. The investigated heavy metal ions showed an inhibitory effect on DNase I activity in a concentration dependent manner with IC50 values of 0.04 μg/mL (Hg2+), 0.10 μg/mL (Pb2+), 1.35 μg/mL (Cd2+), 1.20 μg/mL (As2+), and 1.80 μg/mL (Cu2+). Finally, the new method was applied to detect DNase levels in complicated tumor tissue and cell samples and the results showed that DNase levels increased in tumor tissues compared with that of adjacent tissue.
4.[Genetic Diagnosis and Molecular Therapies for Duchenne Muscular Dystrophy].
Takeshima Y. Rinsho Byori. 2015 Oct;63(10):1194-201.
Duchenne muscular dystrophy (DMD) is the most common form of inherited muscle disease and is characterized by progressive muscle wasting, ultimately resulting in the death of patients in their twenties or thirties. DMD is characterized by a deficiency of the muscle dystrophin as a result of mutations in the dystrophin gene. Currently, no effective treatment for DMD is available. Promising molecular therapies which are mutation-specific have been developed. Transformation of an out-of-frame mRNA into an in-frame dystrophin message by inducing exon skipping is considered one of the approaches most likely to lead to success. We demonstrated that the intravenous administration of the antisense oligonucleotide against the splicing enhancer sequence results in exon skipping and production of the dystrophin protein in DMD case for the first time. After extensive studies, anti-sense oligonucleotides comprising different monomers have undergone clinical trials and provided favorable results, enabling improvements in ambulation of DMD patients.

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