Cl 链霉素可降低通道活性和 Ca2+ 进入的有效部分[3]。

Absorption, Distribution and Excretion
Due to poor oral absorption, aminoglycosides, including streptomycin, are typically administered parenterally. Streptomycin can be administered intramuscularly and, in some cases, intravenously. After an intramuscular injection of 1 gram of streptomycin, peak serum concentrations can reach 25-50 μg/mL within 1 hour. Approximately 50% of streptomycin is excreted in the urine within 24 hours after intravenous or intramuscular injection. After an intramuscular injection of 1 gram of streptomycin sulfate, peak serum concentrations can reach 25-50 μg/mL within 1 hour, slowly decreasing to approximately 50% after 5-6 hours. Significant streptomycin concentrations can be detected in all organs and tissues except brain tissue. Large amounts of streptomycin have been found in pleural effusions and tuberculous cavities. Streptomycin can cross the placenta; serum concentrations in umbilical cord blood are similar to maternal serum concentrations. Small amounts of streptomycin are excreted in breast milk, saliva, and sweat. Streptomycin is not absorbed through the gastrointestinal tract. Streptomycin is rapidly absorbed after intramuscular injection. In adults with normal renal function, after a single intramuscular dose of 1 gram of streptomycin, serum streptomycin concentrations peak within 1 hour, ranging from 25 to 50 μg/mL; serum concentrations decrease by 50% 5-6 hours after administration. A study in preterm infants showed that after an intramuscular injection of 10-11 mg/kg streptomycin, the average serum concentration peaked at approximately 29 μg/mL within 2 hours; the average serum concentration at 12 hours was 11 μg/mL. For more complete data on the absorption, distribution, and excretion of streptomycin (16 items in total), please visit the HSDB record page.

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Metabolism/Metabolites
Aminoglycoside antibiotics are not metabolized and are primarily excreted unchanged in the urine via glomerular filtration. /Aminoglycosides/

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Biological Half-Life
The serum half-life of streptomycin is estimated to be 2.5 hours. In adults with normal renal function, the plasma elimination half-life of streptomycin is typically 2-3 hours; however, in adults with severe renal impairment, the plasma elimination half-life has been reported to reach 110 hours. In premature infants and newborns, the plasma elimination half-life of streptomycin has been reported to be 4-10 hours. Patients with impaired hepatic or renal function have been reported to have a longer plasma elimination half-life than those with isolated renal impairment.

Hepatotoxicity
Intravenous and intramuscular treatment with streptomycin is associated with a mild (asymptomatic) increase in serum alkaline phosphatase, but treatment rarely affects aminotransferase levels or bilirubin, and these changes usually resolve rapidly once streptomycin is discontinued. Only sporadic case reports have shown that streptomycin treatment can cause acute liver injury with jaundice, and these cases were all in combination with other more hepatotoxic anti-tuberculosis drugs (such as isoniazid, pyrazinamide, and rifampin). Streptomycin and aminoglycoside antibiotics were not mentioned in large case series of drug-induced liver disease and acute liver failure; therefore, streptomycin-induced liver injury, if it occurs, is extremely rare. Probability Score: E (Unlikely a clinically obvious cause of liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Similar to other aminoglycoside antibiotics, streptomycin is rarely excreted into breast milk. Neonates appear to absorb small amounts of aminoglycoside antibiotics, but their serum concentrations are far lower than those achieved when treating neonatal infections, making systemic effects of streptomycin unlikely. Older infants are expected to absorb even less streptomycin. Monitoring for potential effects on the infant's gut microbiota is necessary, such as diarrhea, candidiasis (e.g., thrush, diaper rash), or rare hematochezia, which may indicate antibiotic-associated colitis.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
An observational study found that streptomycin did not suppress lactation.

[1]. STREPTOMYCIN, SUPPRESSION, AND THE CODE. Proc Natl Acad Sci U S A. 1964 May;51(5):883-90.

[2]. The Neglected Contribution of Streptomycin to the Tuberculosis Drug Resistance Problem. Genes (Basel). 2021 Dec 17;12(12):2003.

[3]. Streptomycin sulphate loaded solid lipid nanoparticles show enhanced uptake in macrophage, lower MIC in Mycobacterium and improved oral bioavailability. Eur J Pharm Biopharm. 2021 Mar;160:100-124.

Streptomycin is an aminocyclic glycoside composed of streptomycin linked to a disaccharide group at the 4-position. It is the parent compound of streptomycin-type drugs and possesses multiple functions including antibacterial, antimicrobial, antiviral, protein synthesis inhibitor, bacterial metabolite inhibitor, and antifungal pesticide activity. It is an antibiotic, antifungal drug, and bactericide, and a member of the streptomycin family. Its function is related to streptomycin, being the conjugate base of streptomycin (3+). Streptomycin is an antibiotic derived from Streptomyces griseus and was the first aminoglycoside antibiotic discovered and clinically applied in the 1940s. Selman Waxman and Albert Schatz were awarded the Nobel Prize in Physiology or Medicine for their discovery of streptomycin and its antibacterial activity. Although streptomycin was the first antibiotic proven effective against Mycobacterium tuberculosis, due to the emergence of drug resistance, it is no longer widely used and is now mainly used as adjunctive therapy for multidrug-resistant tuberculosis. Streptomycin is an aminoglycoside antibacterial and antimycobacterial drug. Streptomycin is a broad-spectrum aminoglycoside antibiotic commonly used to treat active tuberculosis, but always in combination with other anti-tuberculosis drugs. Streptomycin is often used in combination with drugs known to be hepatotoxic, and its role in liver injury is difficult to assess, but most information suggests that streptomycin is not hepatotoxic. Streptomycin has been reported in Lyngbya majuscula, Senecio, and several other organisms with relevant data. Streptomycin is an aminoglycoside antibiotic derived from Streptomyces griseus and possesses antibacterial activity. Streptomycin irreversibly binds to the 16S rRNA and S12 protein within the bacterial 30S ribosomal subunit. Therefore, the drug interferes with the assembly of the initiation complex between mRNA and the bacterial ribosome, thereby inhibiting the initiation of protein synthesis. Furthermore, streptomycin induces misreading of the mRNA template, leading to frameshift translation and premature termination of translation. This ultimately results in bacterial cell death. Streptomycin is an antibiotic produced by the soil actinomycete Streptomyces griseus. Its mechanism of action is to inhibit the initiation and elongation processes in protein synthesis. See also: streptomycin sulfate (in salt form); streptomycin pantothenate (its active ingredient); streptomycin hydrochloride (its active ingredient).

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Drug Indications
Although streptomycin was the first antibiotic used to treat Mycobacterium tuberculosis infections, it is now primarily used as a second-line treatment due to resistance and toxicity. Streptomycin can also be used to treat a variety of other infections caused by susceptible aerobic strains, especially when other less toxic drugs have failed. Examples include: Yersinia pestis, Tulafrancella, Brucella, Corynebacterium granulomatosa (causing granuloma inguinale and Duchenne granuloma), Haemophilus ducreyi (causing chancroid), Haemophilus influenzae (causing respiratory tract infections, endocarditis, and meningitis, requiring combination with other antibiotics), Klebsiella pneumoniae (causing pneumonia, requiring combination with other antibiotics), Escherichia coli, Proteus, Enterobacter aerogenes, and Klebsiella. Streptococcus pneumoniae and Enterococcus faecalis can cause urinary tract infections. Viridans streptococci and Enterococcus faecalis (in endocarditis, requiring combination with penicillin) can cause Gram-negative bacillus bacteremia (requiring combination with other antibiotics).

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Mechanism of Action
Aminoglycoside drugs enter cells mainly in three stages.
The first "ion-binding phase" occurs when polycationic aminoglycosides bind to negatively charged components of the bacterial cell membrane via electrostatic interactions, such as lipopolysaccharides and phospholipids in the outer membrane of Gram-negative bacteria, and teichoic acid and phospholipids in the cell membrane of Gram-positive bacteria. This binding leads to the displacement of divalent cations, increasing membrane permeability and allowing the aminoglycosides to enter the cell. The second "energy-dependent phase I" of aminoglycoside entry into the cytoplasm depends on the proton kinetic potential and allows small amounts of aminoglycosides to reach their primary intracellular target—the bacterial 30S ribosome. This ultimately leads to protein translation errors and cell membrane disruption. Finally, in "energy-dependent phase II," concentration-dependent bactericidal activity is observed. Due to cell membrane damage, aminoglycosides rapidly accumulate intracellularly, amplifying protein translation errors and inhibitory effects on synthesis. Therefore, aminoglycosides exert both immediate bactericidal effects through cell membrane disruption and delayed bactericidal effects through inhibition of protein synthesis; both observed experimental data and mathematical models support this dual-mechanism model. Inhibition of protein synthesis is a key component of the therapeutic effects of aminoglycosides. Structural and cell biological studies have shown that aminoglycoside antibiotics bind to the 44th helix (h44) of 16S rRNA, located near the A site of the 30S ribosomal subunit, thereby altering the interaction between h44 and h45. This binding also causes a shift in two important residues on h44, A1492 and A1493, mimicking the normal conformational change that occurs when codon-anticodon pairing is successful at the A site. Overall, the binding of aminoglycoside antibiotics has a variety of negative effects, including inhibition of translation, initiation, elongation, and ribosomal cycling. Recent evidence suggests that the latter effect is due to a hidden second binding site at h69 of the 50S ribosomal subunit 23S rRNA. Furthermore, aminoglycoside antibiotics promote mistranslation by stabilizing conformations that mimic correct codon-anticodon pairing. Mistranslated proteins can integrate into the cell membrane, leading to the aforementioned damage. The primary intracellular site of action for aminoglycoside antibiotics is the 30S ribosomal subunit, which consists of 21 proteins and a 16S RNA molecule. At least three proteins, and possibly the 16S ribosomal RNA, are involved in streptomycin binding, and alterations to these molecules can significantly affect streptomycin binding and its subsequent effects. For example, replacing the lysine residue at amino acid position 42 of one ribosomal protein (S12) with asparagine can prevent drug binding; the resulting mutant is completely resistant to streptomycin. Another mutant, with glutamine at that position, is streptomycin-dependent. During protein synthesis, the ribosome selects aminoacyltransferRNA whose anticodon matches the messenger RNA codon at the A site of the small ribosomal subunit. The aminoglycoside antibiotic streptomycin interferes with the decoding process by binding near the codon recognition site. This study used X-ray crystallography to investigate the effect of streptomycin on the decoding site of the 30S ribosomal subunit of Thermophilus thermophilus, which forms a complex with homologous or near-homologous anticodon stem-loop analogs and messenger RNA. Our crystal structures revealed that streptomycin induced significant local aberrations in the 16S ribosomal RNA, including the key bases A1492 and A1493, which are directly involved in codon recognition. Consistent with the kinetic data, we observed that streptomycin stabilizes the near-homologous anticodon stem-loop analog complex while simultaneously disrupting its stability. These data reveal how streptomycin disrupts the recognition of the homologous anticodon stem-loop analog while simultaneously enhancing the recognition of the near-homologous anticodon stem-loop analog. Streptomycin is a widely used antibiotic for treating microbial infections. Its main mechanism of action is to inhibit translation by binding to ribosomes… In early studies of this antibiotic, a mysterious streptomycin-induced potassium efflux phenomenon was observed, which preceded a decrease in cell viability; it was speculated that this efflux altered the electrochemical gradient, making it easier for streptomycin to enter the cytoplasm. Here, we used a high-throughput screening method to search for compounds targeting the mechanosensitive channel (MscL) with high conductivity, and found dihydrostreptomycin in the screening results. Furthermore, we found that MscL is not only essential for the previously reported streptomycin-induced potassium efflux, but also directly enhances the activity of MscL in electrophysiological studies. The data suggest that regulating the MscL channel is a novel mechanism of action for dihydrostreptomycin, and the macropores of MscL may provide a mechanism for drug entry into cells. Aminoglycoside antibiotics are aminocyclic alcohol antibiotics that kill bacteria by inhibiting protein synthesis through binding to 16S rRNA and disrupting the integrity of the bacterial cell membrane. Mechanisms of aminoglycoside resistance include: (a) inactivation of aminoglycosides through N-acetylation, adenylation, or O-phosphorylation; (b) reduction of intracellular aminoglycoside concentrations through alterations in outer membrane permeability, decreased inner membrane transport, active efflux, and drug retention; (c) alteration of the 30S ribosomal subunit target site through mutation; and (d) methylation of the aminoglycoside binding site. .../Aminoglycosides/

C21H39N7O12

581.57

581.265

57-92-1

Streptomycin sulfate;3810-74-0;Penicillin G;61-33-6

19649

White to off-white solid powder

2.0±0.1 g/cm3

872.9±75.0 °C at 760 mmHg

MW: 1457.383. Powder. MP: aproximately 230 °C /Streptomycin sulfate; 3810-74-0/

481.7±37.1 °C

0.0±0.6 mmHg at 25°C

1.762

-2.53

331.43

12

15

9

40

940

15

C[C@H]1[C@@]([C@H]([C@@H](O1)O[C@@H]2[C@H]([C@@H]([C@H]([C@@H]([C@H]2O)O)N=C(N)N)O)N=C(N)N)O[C@H]3[C@H]([C@@H]([C@H]([C@@H](O3)CO)O)O)NC)(C=O)O

UCSJYZPVAKXKNQ-HZYVHMACSA-N

InChI=1S/C21H39N7O12/c1-5-21(36,4-30)16(40-17-9(26-2)13(34)10(31)6(3-29)38-17)18(37-5)39-15-8(28-20(24)25)11(32)7(27-19(22)23)12(33)14(15)35/h4-18,26,29,31-36H,3H2,1-2H3,(H4,22,23,27)(H4,24,25,28)/t5-,6-,7+,8-,9-,10-,11+,12-,13-,14+,15+,16-,17-,18-,21+/m0/s1

2-[(1R,2R,3S,4R,5R,6S)-3-(diaminomethylideneamino)-4-[(2R,3R,4R,5S)-3-[(2S,3S,4S,5R,6S)-4,5-dihydroxy-6-(hydroxymethyl)-3-(methylamino)oxan-2-yl]oxy-4-formyl-4-hydroxy-5-methyloxolan-2-yl]oxy-2,5,6-trihydroxycyclohexyl]guanidine

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~125 mg/mL (~214.94 mM)

注意: 如下所列的是一些常用的体内动物实验溶解配方，主要用于溶解难溶或不溶于水的产品（水溶度<1 mg/mL）。 建议您先取少量样品进行尝试，如该配方可行，再根据实验需求增加样品量。

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注射用配方1: DMSO : Tween 80： Saline = 10 : 5 : 85 (如： 100 μL DMSO → 50 μL Tween 80 → 850 μL Saline)
*生理盐水/Saline的制备：将0.9g氯化钠/NaCl溶解在100 mL ddH ₂ O中，得到澄清溶液。
注射用配方 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL DMSO → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)
注射用配方 3: DMSO : Corn oil = 10 : 90 (如： 100 μL DMSO → 900 μL Corn oil)
示例: 以注射用配方 3 (DMSO : Corn oil = 10 : 90) 为例说明, 如果要配制 1 mL 2.5 mg/mL的工作液, 您可以取 100 μL 25 mg/mL 澄清的 DMSO 储备液，加到 900 μL Corn oil/玉米油中, 混合均匀。

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注射用配方 4: DMSO : 20% SBE-β-CD in Saline = 10 : 90 [如：100 μL DMSO → 900 μL (20% SBE-β-CD in Saline)]
*20% SBE-β-CD in Saline的制备（4°C，储存1周）：将2g SBE-β-CD (磺丁基-β-环糊精) 溶解于10mL生理盐水中，得到澄清溶液。
注射用配方 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (如： 500 μL 2-Hydroxypropyl-β-cyclodextrin (羟丙基环胡精)→ 500 μL Saline)
注射用配方 6: DMSO : PEG300 : Castor oil : Saline = 5 : 10 : 20 : 65 (如： 50 μL DMSO → 100 μL PEG300 → 200 μL Castor oil → 650 μL Saline)
注射用配方 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (如： 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
注射用配方 8: 溶解于Cremophor/Ethanol (50 : 50), 然后用生理盐水稀释。
注射用配方 9: EtOH : Corn oil = 10 : 90 (如： 100 μL EtOH → 900 μL Corn oil)
注射用配方 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (如： 100 μL EtOH → 400 μL PEG300 → 50 μL Tween 80 → 450 μL Saline)

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口服配方 1: 悬浮于0.5% CMC Na (羧甲基纤维素钠)
口服配方 2: 悬浮于0.5% Carboxymethyl cellulose (羧甲基纤维素)
示例: 以口服配方 1 (悬浮于 0.5% CMC Na)为例说明, 如果要配制 100 mL 2.5 mg/mL 的工作液, 您可以先取0.5g CMC Na并将其溶解于100mL ddH2O中，得到0.5%CMC-Na澄清溶液；然后将250 mg待测化合物加到100 mL前述 0.5%CMC Na溶液中，得到悬浮液。

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口服配方 3: 溶解于 PEG400 (聚乙二醇400)
口服配方 4: 悬浮于0.2% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 5: 溶解于0.25% Tween 80 and 0.5% Carboxymethyl cellulose (羧甲基纤维素)
口服配方 6: 做成粉末与食物混合

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注意: 以上为较为常见方法，仅供参考， InvivoChem并未独立验证这些配方的准确性。具体溶剂的选择首先应参照文献已报道溶解方法、配方或剂型，对于某些尚未有文献报道溶解方法的化合物，需通过前期实验来确定（建议先取少量样品进行尝试），包括产品的溶解情况、梯度设置、动物的耐受性等。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。