Aminoglycoside

When applied to different strains of mycobacteria in vitro, kanamycin (0.1-100 μg/mL; 2 weeks) shows good antibacterial activity (MIC=1-5 μg/mL)[1].

In the lung and spleen of mice, kanamycin (2, 4 mg/kg; s.c.; once daily, six times a week for three weeks) inhibits the growth of bovine tubercle bacilli[1]. In addition to increasing the survival rate of mice, kanamycin (1.25, 5 mg/kg; s.c.; single (at 3 h after infection)) inhibits the multiplication of K. pneumonia DT-S in the lung, trachea, and blood of mice and in proportion to the dose administration[2].

Cell Line: mycobacteria H2 and H37RvR-PAS, BCG, Kirchbergand, Ravenel, and H37Rv.
Concentration: 0.1-100 μg/mL
Incubation Time: 2 weeks
Result: demonstrated strong antibacterial activity against multiple mycobacterium strains (H37Rv, H2, H37RvR-PAS, Ravenel, and BCG), with MICs of 1 μg/mL and 5 μg/mL for the Kirchbergand strain, respectively.

Animal Model: Inbred strain normal mice (14-16 g; bovine tubercle bacilli (Ravenel strain) infected model).
Dosage: 2, 4 mg/kg
Administration: Subcutaneous injection: once a day for three weeks, six times a week.
Result: had a noticeable impact on preventing the spread of tuberculosis in vivo, particularly in mice's lungs.

Absorption, Distribution and Excretion
Kanamycin is rapidly absorbed after intramuscular injection, with peak plasma concentrations typically reached within approximately 1 hour. Oral and topical absorption is poor, except in cases of severe skin lesions. A study in preterm infants showed that after a single intramuscular dose of 6.3–8.5 mg/kg of kanamycin, the average peak plasma concentration reached 17.5 μg/mL within 1 hour; after 12 hours, the average plasma concentration was 5.8 μg/mL. In neonates aged 1–7 days, peak plasma concentrations were 21.8 μg/mL and 26.8 μg/mL, respectively, 30 minutes after intramuscular injection of 7.5 mg/kg or 10 mg/kg. When these doses were administered intravenously 20 minutes later, the serum concentrations at 30 minutes were 21.4 and 29.3 μg/mL, respectively. Kanamycin is poorly absorbed from the gastrointestinal tract. In one study, 500 mg of kanamycin dissolved in 20 mL of 0.9% sodium chloride solution and administered intraperitoneally resulted in a peak plasma kanamycin concentration of 19 μg/mL within 15 minutes. Kanamycin is rapidly absorbed after intramuscular injection. In adults with normal renal function, a single intramuscular injection of 7.5 mg/kg of kanamycin resulted in a peak plasma kanamycin concentration of approximately 22 μg/mL within about 1 hour; ¹ 8 hours after administration, the average plasma drug concentration was 3.2 μg/mL. ¹ Similar plasma kanamycin concentrations were achieved 1 hour after intravenous infusion of the same dose. For more complete data on the absorption, distribution, and excretion of kanamycin A (11 in total), please visit the HSDB record page.

---

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

---

Biological Half-Life
2.5 hours

The plasma elimination half-life of kanamycin in adults with normal renal function is 2-4 hours, but the half-life may be prolonged in elderly patients. The average half-life in newborns aged 1-7 days is 4.3-5.1 hours. It has been reported that the average elimination half-life of kanamycin in preterm infants is 9 hours. The plasma half-life and plasma drug concentration may be decreased in patients with severe burns. Patients with renal insufficiency have higher plasma concentrations, and the elimination half-life of kanamycin is prolonged. The plasma half-life of kanamycin in patients with severe renal insufficiency may be 27-80 hours.

Toxicity Summary
Identification and Uses: Kanamycin A is an aminoglycoside antibiotic. Kanamycin injection is indicated for short-term treatment of serious infections caused by susceptible strains of specified microorganisms. Kanamycin may be used as initial treatment when one or more of the following pathogens are known or suspected: Escherichia coli, Proteus spp. (indole-positive and indole-negative), Enterobacter aerogenes, Klebsiella pneumoniae, Serratia marcescens, and Acinetobacter spp. Human Exposure and Toxicity: Kanamycin toxicity to the eighth cranial nerve can cause partial or irreversible bilateral hearing loss, balance disturbances, or both. Tinnitus or vertigo may or may not occur. Cochlear damage typically initially presents as slight changes in high-frequency hearing test results, possibly without subjective hearing loss. Vestibular dysfunction typically presents as nystagmus, vertigo, nausea, vomiting, or acute Meniere's disease. Serious allergic reactions, such as anaphylactic shock and skin reactions including exfoliative dermatitis, toxic epidermal necrolysis, erythema multiforme, angioedema, and Stevens-Johnson syndrome, are rare in patients receiving aminoglycosides; deaths are rare. Cross-sensitivity exists among aminoglycosides. Animal studies: Intravitreal injection of 0.5 mg in rabbits and owl monkeys was well tolerated, but doses of 1.5 to 6.0 mg caused cataracts in rabbits. In pregnant rats and guinea pigs, a daily dose of 200 mg/kg resulted in hearing impairment in offspring.

---

Effects during pregnancy and lactation
◉ Overview of use during lactation
If the mother needs to use kanamycin, breastfeeding does not need to be stopped. Very little kanamycin is excreted into breast milk. Neonates appear to absorb small amounts of other aminoglycoside antibiotics, but even with three daily doses, serum concentrations are far lower than those achieved when treating neonatal infections, so systemic effects of kanamycin are unlikely. Older infants are expected to absorb less kanamycin. Since the concentration of kanamycin in breast milk fluctuates very little with multiple-dose regimens, adjusting breastfeeding and dosing times offers little benefit in reducing infant exposure. Data for once-daily dosing regimens are currently unavailable. Monitor for potential effects on the infant's gut microbiota, such as diarrhea, candidiasis (e.g., thrush, diaper rash), or rare hematochezia, suggesting possible antibiotic-associated colitis.
◉ Effects on Breastfed Infants
Kanamycin was used as part of a six-drug regimen to treat a pregnant woman with multidrug-resistant tuberculosis during early pregnancy and postpartum. The infant was breastfed (the extent and duration of breastfeeding were not specified). The child developed growth retardation at 1.8 years of age, possibly due to postnatal tuberculosis infection, but otherwise developed normally.
◉ Effects on Lactation and Breast Milk
No published information was found as of the revision date.

---

Drug Interactions
Aminoglycosides may cause additive toxicity when used concurrently or sequentially with other systemic, oral, or topical medications that have neurotoxic, ototoxic, or nephrotoxic effects (e.g., other aminoglycosides, acyclovir, amphotericin B, bacitracin, capreomycin, certain cephalosporins, colistin, cisplatin, methoxyflurane, polymyxin B, vancomycin). This should be avoided whenever possible. Aminoglycosides
Because concomitant use of aminoglycosides with potent diuretics (such as ethacrynic acid, furosemide, urea, or mannitol) may increase the risk of ototoxicity due to drug additive effects or changes in serum and tissue aminoglycoside concentrations, aminoglycosides should not be used concomitantly with potent diuretics. Studies have shown that concomitant use of certain antiemetics that suppress vestibular nausea, vomiting, and vertigo (e.g., dimenhydrinate, meclomethasone) may mask the symptoms of aminoglycoside-related vestibular ototoxicity. Concomitant use of aminoglycosides with general anesthetics or neuromuscular blocking agents (e.g., succinylcholine, rocuronium bromide, tubocurarine) may enhance neuromuscular blocking effects and lead to respiratory paralysis. …Aminoglycoside antibiotics should be used with caution in patients receiving anesthetics or neuromuscular blocking agents, and patients should be closely monitored for signs of respiratory depression. /Aminoglycosides/
In vitro studies have shown that the antimicrobial activity of aminoglycosides and β-lactam antibiotics against certain microorganisms, including Enterobacteriaceae, Pseudomonas aeruginosa, Enterococci, and viridans streptococci, may have an additive or synergistic effect. The synergistic effect of aminoglycosides and β-lactam antibiotics has a therapeutic advantage, particularly in treating infections caused by Enterococci or Pseudomonas aeruginosa. Although the exact mechanism of this synergistic effect has not been determined, penicillin appears to allow aminoglycoside antibiotics to enter ribosome binding sites more effectively by inhibiting bacterial cell wall synthesis. Synergistic effects between aminoglycoside antibiotics and broad-spectrum penicillins are often difficult to predict, and antagonistic effects are rarely reported in in vitro studies when these penicillins are used in combination with amikacin, gentamicin, or tobramycin. Therefore, some clinicians recommend that when combination therapy is necessary, appropriate in vitro studies should be conducted to confirm synergistic effects on isolated pathogens. Combination therapy of broad-spectrum penicillins with aminoglycoside antibiotics can lead to decreased serum aminoglycoside concentrations and elimination half-lives, especially in patients with renal impairment. Therefore, serum aminoglycoside concentrations should be monitored in patients receiving combination therapy, especially when using very high doses of broad-spectrum penicillin or in patients with impaired renal function. /Aminoglycosides/
For more complete data on interactions of kanamycin A (10 types), please visit the HSDB records page.

---

Non-human toxicity values
Rat intravenous LD50: 437 mg/kg
Rabbit intravenous LD50: 150 mg/kg
Mouse intravenous LD50: 115 mg/kg
Mouse subcutaneous LD50: 1350 mg/kg
For more complete data on non-human toxicity values of kanamycin A (7 types), please visit the HSDB record page.

[1]. Studies on kanamycin, a new antibiotic against tubercle bacilli. I. Effect on virulent tubercle bacilli in vitro and in mice. J Antibiot (Tokyo). 1957 Nov;10(6):233-5.

[2]. Experimental respiratory tract infection with Klebsiella pneumoniae DT-S in mice: chemotherapy with kanamycin. Antimicrob Agents Chemother. 1980 Mar;17(3):494-505.

[3]. Interaction of kanamycin and related antibiotics with the large subunit of ribosomes and the inhibition of translocation. Biochem Biophys Res Commun. 1978 Sep 29;84(2):358-65.

[4]. Mechanism of inhibition of translocation by kanamycin and viomycin: a comparative study with fusidic acid. Biochem Biophys Res Commun. 1980 Jan 29;92(2):647-54.

Kanamycin A is a member of the kanamycin family, a bacterial metabolite, and the conjugated base of kanamycin A(4+). Kanamycin (also known as kanamycin A) is an aminoglycoside antibiotic available in oral, intravenous, and intramuscular formulations for the treatment of various infections. Kanamycin is isolated from Streptomyces kanamyceticus, and its most commonly used form is kanamycin sulfate. Kanamycin has been reported to be found in Pseudomonas glaucus, Streptomyces, and other organisms with relevant data. Kanamycin is an aminoglycoside antibiotic with antibacterial activity. Amikacin irreversibly binds to the bacterial 30S ribosomal subunit, particularly to the 16S rRNA and S12 protein within the 30S subunit. This disrupts the translation initiation complex, causing misreading of mRNA, thereby inhibiting protein synthesis and producing a bactericidal effect. This drug is commonly used to treat Escherichia coli, Proteus spp. (including indole-positive and indole-negative strains), Enterobacter aerogenes, Klebsiella pneumoniae, Serratia marcescens, and Acinetobacter spp. Kanamycin A is the major component of the kanamycin complex, an aminoglycoside antibiotic isolated from Streptomyces kanamycin, possessing antibacterial activity. This antibiotic complex is produced by Streptomyces kanamycin in Japanese soil. This product consists of three components: the major component, kanamycin A, and minor components, kanamycin B and C. Indications For the treatment of infections known or suspected to be caused by one or more of the following pathogens: Escherichia coli, Proteus spp. (including indole-positive and indole-negative strains), Enterobacter aerogenes, Klebsiella pneumoniae, Serratia marcescens, and Acinetobacter spp. Mechanism of Action Aminoglycoside antibiotics (such as kanamycin) bind irreversibly to specific 30S subunit proteins and 16S rRNA. Specifically, kanamycin binds to four nucleotides of 16S rRNA and one amino acid of the S12 protein. This interferes with the decoding site near nucleotide 1400 in the 30S subunit of the 16S rRNA. This region interacts with the wobble base in the tRNA anticodon. This leads to interference with the initiation complex, misreading of mRNA, resulting in the insertion of incorrect amino acids into the polypeptide chain, producing nonfunctional or toxic peptides, and causing polyribosomes to dissociate into nonfunctional monomeric ribosomes. Kanamycin is an aminoglycoside antibiotic whose mechanism of action is by inhibiting protein synthesis in susceptible microorganisms. It has bactericidal activity against Gram-negative bacteria and some Gram-positive bacteria in vitro. Aminoglycoside antibiotics generally have bactericidal activity. Although their exact mechanism of action is not fully elucidated, this class of drugs appears to inhibit protein synthesis in susceptible bacteria through irreversible binding to the 30S ribosomal subunit. /Aminoglycosides/
…Aminoglycosides 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 through mutation; and (d) methylation of the aminoglycoside binding site. …/Aminoglycosides/

---

Therapeutic Uses
Antibacterial Drugs; Protein Synthesis Inhibitors
/Clinical Trials/ ClinicalTrials.gov is a registry and results database that tracks human clinical studies funded by public and private institutions worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov provides a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure being investigated); the title, description, and design of the study; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as MedlinePlus (providing patient health information) and PubMed (providing citations and abstracts of academic articles in the medical field) from the National Library of Medicine (NLM). Kanamycin A is indexed in this database. Kanamycin injection is indicated for the short-term treatment of serious infections caused by susceptible strains of the following specified microorganisms: /Escherichia coli, Proteus spp. (indole-positive and indole-negative), Enterobacter aerogenes, Klebsiella pneumoniae, Serratia marcescens, Acinetobacter spp./. Bacteriological studies should be performed to identify the causative organism and determine its susceptibility to kanamycin. Treatment may be initiated before susceptibility testing results are obtained. /US Product Label Includes/
Kanamycin may be considered as initial treatment for infections known or suspected to be caused by one or more of the following pathogens: Escherichia coli, Proteus spp. (indole-positive and indole-negative), Enterobacter aerogenes, Klebsiella pneumoniae, Serratia marcescens, Acinetobacter spp. /US Product Label Includes/
For more complete data on the therapeutic uses of kanamycin A (9 in total), please visit the HSDB record page.

---

Drug Warning
/Black Box Warning/ Because aminoglycosides can be toxic, patients receiving aminoglycoside therapy should be closely monitored clinically regardless of the route of administration. As with other aminoglycoside antibiotics, the main toxic effects of kanamycin are its effects on the auditory and vestibular branches of the eighth cranial nerve and the renal tubules. Neurotoxicity manifests as bilateral auditory toxicity, which is usually permanent, and sometimes vestibular ototoxicity. High-frequency hearing loss usually occurs before the appearance of significant clinical hearing loss and can be detected by hearing tests. There may be no clinical symptoms indicating cochlear damage. Dizziness may occur, which could be a sign of vestibular damage. Other neurotoxic manifestations may include numbness, tingling, muscle twitching, and seizures. The risk of hearing loss increases with the peak or trough of blood drug concentration and continues to worsen after discontinuation of the drug. Renal impairment may be characterized by decreased creatinine clearance, the presence of cells or casts in the urine, oliguria, proteinuria, decreased urine specific gravity, or increased nitrogen retention (elevated blood urea nitrogen, non-protein nitrogen, or serum creatinine). Patients with impaired renal function, as well as those with normal renal function receiving high doses or long-term treatment, have a significantly increased risk of severe ototoxicity and nephrotoxicity. Renal function and eighth cranial nerve function should be closely monitored, especially in patients with known or suspected renal impairment at the start of treatment, and in those with initially normal renal function who develop signs of renal dysfunction during treatment. Serum concentrations of parenteral aminoglycosides should be monitored as much as possible to ensure adequate concentrations and avoid potentially toxic levels. Urine should be examined for decreased specific gravity, increased protein excretion, and cells or casts. Blood urea nitrogen, serum creatinine, or creatinine clearance should be monitored regularly. For patients of sufficient age to undergo hearing testing, especially high-risk patients, a series of audiograms should be performed whenever possible. If ototoxicity (dizziness, vertigo, tinnitus, booming in the ears, and hearing loss) or nephrotoxicity symptoms occur, dose adjustment or discontinuation of the drug is necessary. Neuromuscular blockade and respiratory paralysis may occur when kanamycin is administered intraperitoneally with anesthetics and muscle relaxants. Neuromuscular blockade has been reported after parenteral and oral administration of aminoglycosides. The possibility of neuromuscular blockade and respiratory paralysis should be considered if aminoglycosides are administered via any route, especially in patients receiving anesthesia, neuromuscular blocking agents (such as tubocurarine, succinylcholine, or decanoic acid), or large infusions of citrate anticoagulants. If obstruction occurs, calcium salts may help relieve these symptoms, but mechanical ventilation may be required. Concurrent or sequential systemic, oral, or topical administration of kanamycin and other potentially nephrotoxic and/or neurotoxic drugs, especially polymyxin B, bacitracin, colistin, amphotericin B, cisplatin, vancomycin, and all other aminoglycoside antibiotics (including paromomycin), should be avoided as toxicities may be additive. Other factors that may increase the risk of toxicity include advanced age and dehydration. Kanamycin should not be used concurrently with potent diuretics (ethacrynic acid, furosemide, melasmaline, mercaptomeridine, or mannitol). Some diuretics can themselves cause ototoxicity, and intravenous diuretics may enhance the toxicity of aminoglycoside antibiotics by altering serum and tissue antibiotic concentrations. Kanamycin may cause auditory toxicity (and sometimes vestibular toxicity), nephrotoxicity, and neuromuscular blockade. Patients with a history of renal impairment (especially those requiring hemodialysis), those receiving concurrent or sequential treatment with other ototoxic or nephrotoxic drugs or intravenous rapid-acting diuretics (ethacrynic acid, furosemide, and mannitol), and those receiving prolonged treatment and/or at doses higher than the recommended dose are at higher risk. Local irritation or pain may occur after intramuscular injection of kanamycin. Other rare adverse reactions include rash, drug fever, headache, paresthesia, nausea, vomiting, and diarrhea. Long-term use of kanamycin has been reported to cause "malabsorption syndrome," characterized by increased fecal fat, decreased serum carotene, and decreased xylose absorption. Proteinuria, the presence of red and white blood cells and granular casts in the urine, azotemia, and oliguria have been reported. Renal function changes are usually reversible after discontinuation of kanamycin. Renal impairment may be characterized by elevated serum creatinine, possibly accompanied by oliguria, the presence of casts, cells, and proteins in the urine, elevated blood urea nitrogen levels, or decreased creatinine clearance. For more complete data on drug warnings for kanamycin A (32 in total), please visit the HSDB records page.

---

Pharmacodynamics
Kanamycin is an aminoglycoside antibiotic. Aminoglycosides work by binding to the 30S ribosomal subunit of bacteria, causing tRNA misreading and preventing the bacteria from synthesizing proteins essential for their growth. Aminoglycosides are primarily used to treat infections caused by aerobic Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including those that cause tuberculosis, are also sensitive to aminoglycosides. Gram-positive bacterial infections can also be treated with aminoglycosides, but other types of antibiotics are more effective and less harmful to the host. In the past, aminoglycosides have been used in combination with penicillins to treat streptococcal infections because of their synergistic effect, particularly in the treatment of endocarditis. Aminoglycosides are largely ineffective against anaerobes, fungi, and viruses.

C18H36N4O11

484.503

484.238

C, 44.62; H, 7.49; N, 11.56; O, 36.32

59-01-8

Kanamycin sulfate;25389-94-0

6032

White to off-white solid powder

1.6±0.1 g/cm3

809.5±65.0 °C at 760 mmHg

443.4±34.3 °C

0.0±6.5 mmHg at 25°C

1.670

-2.58

11

15

6

33

638

15

C1[C@H]([C@@H]([C@H]([C@@H]([C@H]1N)OC2[C@@H]([C@H]([C@@H]([C@@H](CN)O2)O)O)O)O)O[C@@H]3[C@@H]([C@H]([C@@H]([C@@H](CO)O3)O)N)O)N

SBUJHOSQTJFQJX-NOAMYHISSA-N

InChI=1S/C18H36N4O11/c19-2-6-10(25)12(27)13(28)18(30-6)33-16-5(21)1-4(20)15(14(16)29)32-17-11(26)8(22)9(24)7(3-23)31-17/h4-18,23-29H,1-3,19-22H2/t4-,5+,6-,7-,8+,9-,10-,11-,12+,13-,14-,15+,16-,17-,18-/m1/s1

(2R,3S,4S,5R,6R)-2-(aminomethyl)-6-(((1R,2R,3S,4R,6S)-4,6-diamino-3-(((2S,3R,4S,5S,6R)-4-amino-3,5-dihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl)oxy)-2-hydroxycyclohexyl)oxy)tetrahydro-2H-pyran-3,4,5-triol

Kanamycin A; Kanamycin free base; Kanamycin A; Kantrex; Kanamycine.

2941.90.1010

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

---

Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

View More

Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

---

Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

View More

Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

---

Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

---

 (Please use freshly prepared in vivo formulations for optimal results.)