50S subunit of the bacterial ribosome, which inhibits bacterial protein synthesis

Clindamycin demonstrates potent in vitro antibacterial activity against a range of pathogens. Its antibacterial activity against aerobic Gram-positive bacteria is 4 to 8 times stronger than its precursor, lincomycin. It is highly active against anaerobes, including Bacteroides fragilis, Clostridium perfringens, and Peptostreptococcus. For instance, the minimum inhibitory concentration (MIC) of clindamycin against Staphylococcus aureus is typically below 0.5 μg/mL, while against Bacteroides fragilis, the MIC ranges from 0.25 to 4 μg/mL. Notably, partial cross-resistance exists between clindamycin and macrolides, while complete cross-resistance exists with lincomycin.

In animal models, the in vivo activity of clindamycin is consistent with or even superior to its in vitro activity. After oral administration, clindamycin is rapidly absorbed with good bioavailability (approximately 72.55% in dogs) and is widely distributed in body fluids and tissues (steady-state volume of distribution is approximately 2.48 L/kg). In mice with experimental infections caused by Staphylococcus aureus or Streptococcus hemolyticus, clindamycin showed a much better in vivo protective effect than lincomycin. In a canine periodontitis model, clindamycin hydrochloride significantly reduced halitosis, plaque, and gingival bleeding, and achieved a 71.4% complete remission rate for superficial bacterial pyoderma.

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In a clinical study of 21 dogs with canine superficial bacterial pyoderma, oral administration of clindamycin at approximately 11 mg/kg body weight once daily for 14 to 42 days resulted in an excellent clinical response (complete remission) in 71.4% (15/21) of dogs within 14 to 28 days [2].
In vitro susceptibility testing of Staphylococcus intermedius isolates from dogs with superficial pyoderma showed that 14 out of 18 isolates (77.8%) were susceptible to clindamycin, 4 were resistant [2].
In six nonresponder dogs, follow-up cultures revealed that three dogs with initial clindamycin-susceptible S. intermedius isolates developed resistance during therapy; one dog with initially intermediate susceptibility developed resistance; two dogs had initial resistance [2].

To investigate the binding kinetics of clindamycin to the ribosome, chemical footprinting is employed. Purified bacterial ribosomes (70S or 50S subunits) are typically used. Clindamycin is incubated with the ribosomal complex in a specific buffer for a very short time (e.g., 1 second) to capture the initial encounter complex (CI), or for 1 minute to form the stabilized complex (C*I). Subsequently, chemical modifying agents (e.g., DMS or kethoxal) are added to modify unprotected nucleotides. Protected sites on the ribosomal RNA are detected by primer extension reverse transcriptase analysis. For instance, studies have shown that clindamycin protects nucleotides A2058 and A2059, as well as residues within the peptidyl transferase center like A2451 and G2505, revealing its binding sites.

In vitro cellular assays for clindamycin often employ eukaryotic cell lines (such as human hepatoma HepG2 cells or immune cells) to assess its cytotoxicity or effects on cell function. Cells are cultured to log phase in media containing 10% fetal bovine serum and seeded into 96-well plates. After overnight incubation, cells are treated with gradient concentrations of clindamycin (e.g., 0-1000 μg/mL) for 24 to 72 hours. Cell viability is then measured using MTT or CCK-8 assays, with absorbance read using a microplate reader. Additionally, HIV-infected MOLT3 cell models can be used to assess whether clindamycin exacerbates cell death. These assays help determine the safe concentration range of the drug.

Classic animal models for evaluating clindamycin pharmacokinetics and pharmacodynamics are dogs or mice. In canine studies, a two-period crossover design is often used. Clindamycin hydrochloride is administered either intravenously (e.g., 11 mg/kg) or orally (e.g., 150 mg capsule). Blood samples are collected from a vein at multiple time points post-administration (e.g., 0, 0.5, 1, 2, 4, 8, 12, 24 hours). Serum is separated by centrifugation, and drug concentrations are determined using HPLC or LC-MS/MS to calculate pharmacokinetic parameters such as clearance, volume of distribution, and bioavailability. For infection models, mice can be challenged intraperitoneally with a lethal dose of Staphylococcus aureus and then treated subcutaneously with clindamycin, with animal survival recorded over 7-14 days.

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For the clinical efficacy study in dogs with superficial bacterial pyoderma, clindamycin was administered orally at approximately 11 mg/kg body weight once daily (q24h). The dosage ranged from 10.5 to 12.9 mg/kg body weight, with a mean dosage of 11.34 mg/kg and a median of 11.1 mg/kg. Duration of therapy was 14 to 42 days, determined by clinical response. Dogs were reexamined on days 14, 28, and if necessary day 42. No topical therapies (including bathing) or other systemic therapies (corticosteroids, antihistamines, fatty-acid supplements, allergen injections) were allowed during the study [2].
For the pharmacokinetic study in dogs, six healthy male Beagle dogs (12-17 kg, 12 months old) were used. Clindamycin hydrochloride was administered intravenously at 11 mg/kg body weight via catheterization of the left cephalic vein. Blood samples were collected at 0, 2, 5, 10, 15, 20, 30, 45 min, 1, 1.5, 2, 2.5, 3, 4, 5, 6, 8, 10, 12, and 24 h post-dose. For oral administration, dogs received one 150 mg clindamycin hydrochloride capsule, with dose normalized to mg/kg by dividing total clindamycin received by body weight. Blood samples were collected at 0, 15, 30, 45 min, 1, 1.5, 2, 2.5, 3, 4, 5, 6, 8, 10, 12, and 24 h post-dose. All animals were fasted for 12 h before each drug administration. A four-week wash-out interval separated the two treatment periods [1].

Absorption, Distribution and Excretion
Oral bioavailability is nearly complete, approximately 90%, with a mean peak serum concentration (Cmax) of 2.50 µg/mL and a time to peak concentration (Tmax) of 0.75 hours. The AUC after an oral dose of 300 mg is approximately 11 µg•hr/mL. Systemic exposure after vaginal suppository administration is 40 to 50 times lower than after parenteral administration, and the peak plasma concentration (Cmax) after vaginal cream administration is only 0.1% of that after parenteral administration. Approximately 10% of the bioactive substance of clindamycin is excreted in the urine, 3.6% in the feces, and the remainder as inactive metabolites. Clindamycin is widely distributed throughout the body, including in bones, but not in cerebrospinal fluid. Its volume of distribution is estimated to be between 43 and 74 liters. The plasma clearance of clindamycin is estimated to be 12.3–17.4 L/h, with decreased plasma clearance in patients with cirrhosis and altered plasma clearance in patients with anemia.
Clindamycin is almost completely absorbed after oral administration. After a 150 mg dose, peak plasma concentrations can reach 2 to 3 μg/mL within 1 hour. The presence of food in the stomach does not affect absorption. The antibiotic has a half-life of approximately 2.9 hours; therefore, if administered every 6 hours, drug accumulation is not expected. Clindamycin is widely distributed in various body fluids and tissues, including bone. Even in cases of meningitis, significant concentrations are not reached in the cerebrospinal fluid. Concentrations required for treating cerebral toxoplasmosis are achievable. The drug readily crosses the placental barrier. 90% or more of clindamycin binds to plasma proteins. Clindamycin accumulates in polymorphonuclear leukocytes, alveolar macrophages, and abscesses.
Half-life…only slightly prolonged in patients with significantly impaired renal function…
Clindamycin is distributed in various body fluids and tissues, including saliva, ascites, pleural fluid, synovial fluid, bone, and bile. However, even in cases of meningitis, only a small amount of the drug diffuses into the cerebrospinal fluid. Clindamycin concentrations in synovial fluid and bone are reported to be approximately 60-80% of the corresponding serum concentrations; its permeability appears unaffected by joint inflammation. Clindamycin readily crosses the placenta; umbilical cord blood concentrations are reported to be approximately 46% of the corresponding maternal blood concentrations. Clindamycin is secreted into breast milk. For more complete data on the absorption, distribution, and excretion of clindamycin (24 in total), please visit the HSDB records page. Metabolism/Metabolites Clindamycin is primarily metabolized in the liver via CYP3A4, with less metabolic activity via CYP3A5. Two inactive metabolites have been identified—an oxidative metabolite, clindamycin sulfoxide; and an N-demethylated metabolite, N-demethylclindamycin. Clindamycin is partially metabolized into biologically active and inactive metabolites. The main biologically active metabolites are clindamycin sulfoxide and N-demethylclindamycin, which are excreted in urine, bile, and feces. Within 24 hours after oral administration of clindamycin, approximately 10% is excreted in the urine, 3.6% is excreted in the feces as the active drug and its metabolites; the remainder is excreted as inactive metabolites. Only about 10% of clindamycin is excreted unchanged in the urine, with a small amount present in the feces… Clindamycin is metabolized to N-demethylclindamycin and clindamycin sulfoxide, excreted in the urine and bile. Known human metabolites of clindamycin include N-demethylclindamycin and clindamycin sulfoxide. Biological Half-Life The elimination half-life of clindamycin in adults is approximately 3 hours, and in children approximately 2.5 hours. The half-life is prolonged to approximately 4 hours in the elderly. The serum half-life of clindamycin in adults and children with normal renal function is 2–3 hours. In patients with significantly impaired renal or hepatic function, the serum half-life is slightly prolonged. The serum half-life in newborns depends on gestational age, chronological age, and birth weight. Reports indicate that the average serum half-life of clindamycin in preterm infants and full-term newborns is 8.7 hours and 3.6 hours, respectively, while the serum half-life in infants aged 4 weeks to 1 year is approximately 3 hours; infants weighing less than 3.5 kg have a longer serum half-life than heavier infants. The half-life of clindamycin is approximately 2.9 hours. After intravaginal application of 2% clindamycin cream, the systemic half-life of the drug is approximately 1.5–2.6 hours. After intravaginal application of clindamycin suppositories, the average apparent elimination half-life is approximately 11 hours (range: 4–35 hours).

Hepatotoxicity
Clindamycin is associated with two types of hepatotoxicity: one is a transient increase in serum transaminases, usually occurring several days after intravenous administration of high-dose clindamycin; the other is acute specific liver injury, which usually occurs within 1 to 3 weeks after the start of treatment and is generally mild and self-limiting. High-dose intravenous clindamycin can cause serum ALT levels to rise to 2 to 10 times the upper limit of normal, usually occurring 5 to 15 days after treatment, similar to intravenous oxacillin (Case 1). Symptoms, jaundice, and elevated alkaline phosphatase, if present, are mild (Case 2), and transaminase levels return to normal rapidly within 1 to 2 weeks after discontinuation of clindamycin or switching to a lower dose or oral formulation (this is rare). Clindamycin treatment is also associated with clinically significant specific liver injury, which usually occurs within 1 to 3 weeks after the start of oral or parenteral administration (Case 3). The pattern of serum enzyme elevation is usually hepatocellular or mixed, but it can also be cholestatic. Allergic reactions such as rash, fever, and eosinophilia are typical but usually subtle and not present in all cases. Autoantibodies are generally not present. Acute liver injury may be accompanied by other signs of hypersensitivity reactions, such as Stevens-Johnson syndrome or other severe skin reactions. Liver injury is usually mild to moderate and recovers rapidly after discontinuation of the drug. However, fatal cases have been reported. Probability score: B (Very likely to cause clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Clindamycin may have adverse effects on the gut microbiota of breastfed infants. If a breastfeeding mother requires oral or intravenous clindamycin, this is not a reason to discontinue breastfeeding, but may preclude the use of other medications. The infant's gut microbiota should be monitored for potential effects, such as diarrhea, candidiasis (thrush, diaper rash), or rare rectal bleeding, suggesting possible antibiotic-associated colitis. Vaginal administration is unlikely to cause side effects in infants, although approximately 30% of the vaginal dose is absorbed. Topical application of medications to treat acne is unlikely to cause side effects in infants; however, if ingested by an infant, topical application to the breasts may increase the risk of diarrhea. Only water-soluble creams, foams, gels, or liquid products should be applied to the breasts, as ointments may expose the infant to high concentrations of mineral oil through licking.
◉ Effects on Breastfed Infants
A 5-day-old breastfed infant developed bloody stools, possibly due to the mother's concurrent intravenous administration of clindamycin 600 mg (every 6 hours) and gentamicin 80 mg (every 8 hours). The infant's stool flora was reported to be normal, and the fecal occult blood test turned negative 24 hours after breastfeeding was discontinued. The infant resumed breastfeeding on day 6 after the mother discontinued antibiotics without further difficulties.
◉ Effects on Lactation and Breast Milk
No relevant published information was found as of the revision date.
◈ What is Clindamycin?
Clindamycin is an antibiotic used to treat or prevent bacterial infections. It can be taken orally, topically, or intravenously. Sometimes, when people find out they are pregnant, they consider changing their medication regimen or even stopping it entirely. However, it is essential to consult your healthcare provider before changing your medication regimen. Your healthcare provider can discuss with you the benefits of treating your condition and the risks of not treating it during pregnancy.
◈ I am taking clindamycin. Will taking clindamycin affect my pregnancy?
It is currently unclear whether clindamycin affects pregnancy.
◈ Does taking clindamycin increase the risk of miscarriage?
Miscarriage is common and can occur in any pregnancy for a variety of reasons. One study of 249 women with vaginal bacterial infections found that clindamycin treatment reduced the risk of late miscarriage.
◈ Does taking clindamycin increase the risk of birth defects?
The probability of a birth defect at the start of each pregnancy is approximately 1 in 33 (3%). This is known as the background probability. Taking clindamycin is unlikely to increase the risk of birth defects. Multiple human and animal studies have not shown an increased risk of birth defects. When clindamycin is applied to the skin (topical application), only a small amount of the drug enters the bloodstream through the skin. This means that pregnant women will only be exposed to a very small amount of the drug. Since existing information on vaginal and oral clindamycin (both of which have higher absorption rates than topical application) has not found an increased risk of birth defects, topical clindamycin is unlikely to increase the risk of birth defects either.
◈ Does taking clindamycin during pregnancy increase the risk of other pregnancy-related problems?
Multiple studies have not found that taking clindamycin during pregnancy increases the risk of other pregnancy-related problems, such as low birth weight (birth weight less than 5 pounds 8 ounces [2500 grams]). One study involving 249 women with vaginal bacterial infections found that clindamycin treatment reduced the risk of preterm birth (delivery before 37 weeks of gestation).
◈ Will taking clindamycin during pregnancy affect a child's future behavior or learning abilities?
Currently, there are no studies exploring whether clindamycin causes behavioral or learning problems in children.
◈ Breastfeeding while taking clindamycin:
When a woman takes clindamycin orally or intravenously, a small amount of clindamycin may enter breast milk. In this case, clindamycin may cause some gastrointestinal reactions in breastfeeding women (such as nausea, diarrhea, stomach pain, vomiting, diaper rash, thrush, or, in rare cases, rectal bleeding). Topical application (applied to the skin) results in very little absorption and is unlikely to enter breast milk, therefore it is unlikely to cause side effects in a breastfeeding infant. If you notice any symptoms in your child, contact their healthcare provider. Be sure to discuss all questions about breastfeeding with your healthcare provider.
◈ Does clindamycin affect fertility or increase the risk of birth defects if the man takes it?
Currently, no studies have explored whether clindamycin affects male fertility (the ability to impregnate a partner) or increases the risk of birth defects (above background risk). Generally, contact with the father or sperm donor is unlikely to increase the risk of pregnancy. For more information, please refer to the "Paternal Exposure" information sheet on the MotherToBaby website: https://mothertobaby.org/fact-sheets/paternal-exposures-pregnancy/.

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Protein Binding
The protein binding rate of clindamycin is concentration-dependent, ranging from 60-94%. It primarily binds to α-1-acid glycoprotein in serum.

[1]. Clindamycin bioavailability and pharmacokinetics following oral administration of clindamycin hydrochloride capsules in dogs. Vet J. 2005 Nov;170(3):339-45.

[2]. Efficacy of once-daily clindamycin hydrochloride in the treatment of superficial bacterial pyoderma in dogs. J Am Anim Hosp Assoc. 2001 Nov-Dec;37(6):537-42.

[3]. Effect of clindamycin hydrochloride on oral malodor, plaque, calculus, and gingivitis in dogs with periodontitis. Vet Ther. 2000 Winter;1(1):5-16.

[4]. Effects of treatment with clindamycin hydrochloride on progression of canine periodontal disease after ultrasonic scaling. Vet Ther. 2000 Summer;1(3):150-8.

Clindamycin is a semi-synthetic lincosamide antibiotic used to treat a variety of serious infections caused by susceptible microorganisms and can also be used topically to treat acne vulgaris. Its antibacterial spectrum is relatively narrow, including anaerobic bacteria, Gram-positive cocci and bacilli, and Gram-negative bacilli. Interestingly, clindamycin appears to have some activity against protozoa and has been used to treat toxoplasmosis, malaria, and babesiosis (off-label use). Clindamycin is derived from naturally occurring lincomycin and has largely replaced it due to its superior properties compared to the parent compound. Lincomycin is a naturally occurring lincosamide antibiotic and is representative of this class. The name lincomycin comes from Lincoln, Nebraska, where it was initially isolated from Streptomyces lincolnensis found in soil samples. Clindamycin is a lincosamide antibacterial drug. Its physiological effects are achieved by reducing sebaceous gland activity and through neuromuscular blockade. Clindamycin is a broad-spectrum antibiotic available for oral, topical, and parenteral administration to treat bacterial infections caused by susceptible bacteria. Clindamycin has been associated with rare cases of acute liver injury. Clindamycin is a semi-synthetic broad-spectrum antibiotic, chemically modified from the parent compound lincomycin. Clindamycin causes peptidyl-tRNA to dissociate from bacterial ribosomes, thereby disrupting bacterial protein synthesis. (NCI04) An antibacterial agent, a semi-synthetic analogue of lincomycin. See also: Clindamycin phosphate (salt form); Clindamycin hydrochloride (salt form); Clindamycin palmitate (salt form)...see more...

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Drug Indications
Clindamycin, both oral and injectable formulations, is indicated for the treatment of serious infections caused by susceptible anaerobes, as well as susceptible Staphylococcus, Streptococcus, and Pneumococcus. When used topically, clindamycin is indicated for the treatment of acne vulgaris, and may be used in combination with benzoyl peroxide or retinoic acid, or with benzoyl peroxide and adapalene. Clindamycin is also available as a vaginal cream, suppository, or gel for the treatment of bacterial vaginosis in non-pregnant women. Clindamycin is used to prevent viridans streptococcal infections in susceptible patients undergoing oral, dental, or upper respiratory tract surgery, and can also be used to prevent bacterial endocarditis in patients with penicillin allergies and at high risk of infection.
FDA Label

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Mechanism of Action
Clindamycin inhibits bacterial protein synthesis by binding to the 23S RNA of the 50S subunit of the bacterial ribosome. It inhibits both ribosome assembly and translation. The molecular mechanism by which clindamycin exerts its effect is thought to be related to its three-dimensional structure, which is very similar to the 3' end structure of L-Pro-Met-tRNA and deacylated tRNA in the peptide chain elongation cycle—as a structural analogue of these tRNA molecules, clindamycin inhibits peptide chain initiation and may promote the dissociation of peptidyl-tRNA from bacterial ribosomes. The mechanism of topical application of clindamycin for the treatment of acne vulgaris is unclear, but it may be related to its activity against Propionibacterium acnes, an acne-associated bacterium. The effect of clindamycin may be bacteriostatic or bactericidal, depending on the drug concentration at the site of infection and the susceptibility of the infecting microorganism. Clindamycin palmitate and clindamycin phosphate are inactive until hydrolyzed into free clindamycin. This hydrolysis occurs rapidly in vivo. Clindamycin appears to inhibit protein synthesis in susceptible organisms by binding to the 50S ribosomal subunit; its primary action is the inhibition of peptide bond formation. Its site of action appears to be the same as that of erythromycin, chloramphenicol, and lincomycin. Clindamycin specifically binds to the 50S subunit of the bacterial ribosome and inhibits protein synthesis. ...Clindamycin is not a substrate of the macrolide efflux pump; therefore, strains resistant to macrolides through this mechanism are susceptible to clindamycin.

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Clindamycin is a semi-synthetic lincosamide antibiotic derived from lincomycin by substitution of a hydroxyl group with chlorine at the C7 position. It has superior antimicrobial activity against Gram-positive aerobes (cocci and bacteria) and anaerobic bacteria compared to lincomycin. MICs for susceptible strains generally range from 0.04 to 0.5 μg/mL [1].
Clindamycin is effective against Staphylococcus intermedius, the most common infectious organism isolated in cases of canine superficial bacterial folliculitis [2].
For time-dependent antimicrobial agents such as clindamycin, serum concentrations should remain above the MIC of pathogen microorganisms for at least 40-50% of the dosing interval. Clindamycin serum concentrations after IV and oral administration remain above 0.5 μg/mL for approximately 10 h [1].
The authors recommend that for the most susceptible microorganisms (MIC50 ≤0.5 μg/mL), an oral dosage of 11 mg/kg once daily is likely therapeutically effective; for less susceptible bacteria (MIC50 0.5-2 μg/mL), the same dose should be given twice daily [1].
Clindamycin has been shown to display concentration-independent bactericidal activity and exhibits an in vitro post-antibiotic effect of 0.4-3.9 h for Staphylococcus aureus and 2 h for Bacillus anthracis. In vivo, the post-antibiotic effect is generally longer (e.g., 7.1 h against S. aureus in neutropenic mouse thigh model) [1].

C18H33CLN2O5S

424.98

424.179

C, 50.87; H, 7.83; Cl, 8.34; N, 6.59; O, 18.82; S, 7.54

18323-44-9

Clindamycin hydrochloride;21462-39-5;Clindamycin phosphate;24729-96-2;Clindamycin-d3 hydrochloride;1356933-72-6;Clindamycin-13C,d3;2140264-63-5;Clindamycin hydrochloride monohydrate;58207-19-5

446598

Yellow, amorphous solid

1.3±0.1 g/cm3

628.1±55.0 °C at 760 mmHg

141 - 143ºC

333.6±31.5 °C

0.0±4.2 mmHg at 25°C

1.574

1.83

4

7

7

27

502

9

CCC[C@@H]1C[C@H](N(C1)C)C(N[C@@H]([C@@H]2[C@H](O)[C@H](O)[C@@H](O)[C@@H](SC)O2)[C@@H](Cl)C)=O

KDLRVYVGXIQJDK-AWPVFWJPSA-N

InChI=1S/C18H33ClN2O5S/c1-5-6-10-7-11(21(3)8-10)17(25)20-12(9(2)19)16-14(23)13(22)15(24)18(26-16)27-4/h9-16,18,22-24H,5-8H2,1-4H3,(H,20,25)/t9-,10+,11-,12+,13-,14+,15+,16+,18+/m0/s1

(2S,4R)-N-((1S,2S)-2-chloro-1-((2R,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(methylthio)tetrahydro-2H-pyran-2-yl)propyl)-1-methyl-4-propylpyrrolidine-2-carboxamide

U-21251; U 21251; U21251; U-21,251; U 21,251; U21,251; Clindamycin; Cleocin, Clinacin, Dalacin

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

DMSO : ~125 mg/mL (~294.13 mM)

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.

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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).

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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)

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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).

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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

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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.

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