HSV-1 (IC50 = 2.9 μg/mL)

Valaciclovir (VACV) has maximal rates of 23.34 nmol/mg protein/5 minutes and 1.64 mM, respectively, according to Michaelis-Menten constants, with concentration-dependent and saturable absorption. The Km values in rat, rabbit, and Caco-2 cells, as well as in hPEPT1/CHO cells, were quite similar, suggesting that hPEPT1 controls the in vitro intestinal transport characteristics of VACV [5].

A major comparative trial found that valacyclovir (1 g twice day) for 10 days was just as effective as acyclovir (200 mg 5 times daily) for treating a first bout of genital herpes. Two trials found that valacyclovir (200 mg five times daily) was equally efficacious as acyclovir (200 mg five times daily) in a five-day treatment cycle for managing relapses. Valacyclovir at a dose of 1 g per day works just as well as 2 g per day. One dose of valacyclovir can be given every day [1]. Serum and cerebrospinal fluid acyclovir concentrations were assessed at steady state following six days of oral valacyclovir 1,000 mg three times a day [2]. PE and AC have EC50 values in 3T3 cells of 0.02 and 0.01 ug/ml, however in BHK cells they are 0.2 and 0.03 ug/ml. Immunosuppressed mice that were infected were treated with FA and VA (bid, 5.5 days) to eradicate otoparesis, ear lesions (vesicles, etc.), and death. The percentage of erythema was also reduced from 100% to 24% and 38%. By day six, the virus had vanished from the ears and brainstem, but in mice receiving VA treatment, it returned when the medication was stopped [3].

The in vitro 50% inhibitory concentration (IC50) of HSV-1 W strain was determined by using a plaque-reduction assay to verify its sensitivity to acyclovir. The IC50 for HSV-1 W was determined to be 2.9 µg/ml. [4].

The results of previous work performed in our laboratory using an in situ perfusion technique in rats and rabbit apical brush border membrane vesicles have suggested that the intestinal uptake of valacyclovir (VACV) appears to be mediated by multiple membrane transporters. Using these techniques, it is difficult to characterize the transport kinetics of VACV with each individual transporter in the presence of multiple known or unknown transporters. The purpose of this study was to characterize the interaction of VACV and the human intestinal peptide transporter using Chinese hamster ovary (CHO) cells that overexpress the human intestinal peptide transporter (hPEPT1) gene. VACV uptake was significantly greater in CHO cells transfected with hPEPT1 than in cells transfected with only the vector, pcDNA3. The optimum pH for VACV uptake was determined to occur at pH 7.5. Proton cotransport was not observed in hPEPT1/CHO cells, consistent with previously observed results in tissues and Caco-2 cells. VACV uptake was concentration dependent and saturable with a Michaelis-Menten constant and maximum velocity of 1.64 +/- 0.06 mM and 23.34 +/- 0.36 nmol/mg protein/5 min, respectively. A very similar Km value was obtained in hPEPT1/CHO cells and in rat and rabbit tissues and Caco-2 cells, suggesting that hPEPT1 dominates the intestinal transport properties of VACV in vitro. VACV uptake was markedly inhibited by various dipeptides and beta-lactam antibiotics, and Ki values of 12.8 +/- 2.7 and 9.1 +/- 1.2 mM were obtained for Gly-Sar and cefadroxil at pH 7.5, respectively. The present results demonstrate that VACV is a substrate for the human intestinal peptide transporter in hPEPT1/CHO cells and that although transport is pH dependent, proton cotransport is not apparent. Also, the results demonstrate that the hPEPT1/CHO cell system has use in investigating the transport kinetics of drugs with the human intestinal peptide transporter hPEPT1; however, the extrapolation of these transport properties to the in vivo situation requires further investigation[5].

Acyclovir has been a frequently used antiviral agent in the clinical treatment of leukemia, acute encephalitis, malignant tumor and herpes simplex. The adverse effects of this drug have been widely described in clinical practice. In the present study, a case of a 35-year-old female patient diagnosed with herpes simplex, who developed acute renal injury following treatment with valacyclovir hydrochloride, is described. Kidney biopsy, light microscopy and laboratory examination were performed, and all findings revealed the signs of evident vacuolar degeneration of capillary endothelial and renal tubular epithelial cells, erythrocyte aggregation in partial renal tubule and microvilli exfoliation from epithelial cells. Renal interstitial edema was clearly identified. The clinical evidence observed from this female patient indicated that renal functions should be closely monitored during valacyclovir hydrochloride administration. A variety of effective measures, such as hydration, alkalizing urine, promoting the discharge of medication and the use of antagonists are recommended following the administration of antiviral agents[1].

Absorption, Distribution and Excretion
After oral administration, valacyclovir hydrochloride is rapidly absorbed from the gastrointestinal (GI) tract and converted to acyclovir and L-valine. The absolute bioavailability of acyclovir after administration of valacyclovir was measured at 54.5% ± 9.1% after the administration of a 1 gram oral dose of valacyclovir and a 350 mg intravenous (IV) acyclovir dose to 12 healthy subjects. Acyclovir (a metabolite of valacyclovir) bioavailability from the administration of this drug is not affected by the administration with food.
After oral administration of a single 1 gram dose of radiolabeled valacyclovir to 4 healthy subjects, 46% and 47% of administered radioactivity was measured in urine and feces, respectively, over 96 hours. Acyclovir accounted for 89% of the radioactivity excreted in the urine.
Cerebrospinal fluid (CSF) penetration, determined by CSF/plasma AUC ratio, is approximately 25% for aciclovir and the metabolite _8-hydroxy-aciclovir_ (8-OH-ACV), and approximately 2.5% for the metabolite _9-(carboxymethoxy)methylguanine_. In a study of immunocompromised pediatric patients, the volume of distribution of a 15 ml/kg dose of valacyclovir was 1.34 ± 0.65 L/kg.
Renal clearance of acyclovir following the administration of a single 1 gram dose of valacylcovir to 12 healthy 437 volunteers was approximately 255 ± 86 mL/min, which represents 42% of total acyclovir apparent plasma clearance.
After oral administration, valacyclovir hydrochloride is rapidly absorbed from the gastrointestinal tract and nearly completely converted to acyclovir and L-valine by first-pass intestinal and/or hepatic metabolism. The absolute bioavailability of acyclovir after administration of Valtrex is 54.5% + or - 9.1% as determined following a 1-gram oral dose of Valtrex and a 350 mg intravenous acyclovir dose to 12 healthy volunteers. Acyclovir bioavailability from the administration of Valtrex is not altered by administration with food (30 minutes after an 873 Kcal breakfast, which included 51 grams of fat).
The binding of valacyclovir to human plasma proteins ranges from 13.5% to 17.9%. The binding of acyclovir to human plasma proteins ranges from 9% to 33%.
The pharmacokinetic disposition of acyclovir delivered by valacyclovir is consistent with previous experience from intravenous and oral acyclovir. Following the oral administration of a single 1 gram dose of radiolabeled valacyclovir to 4 healthy subjects, 46% and 47% of administered radioactivity was recovered in urine and feces, respectively, over 96 hours. Acyclovir accounted for 89% of the radioactivity excreted in the urine. Renal clearance of acyclovir following the administration of a single 1-gram dose of Valtrex to 12 healthy volunteers was approximately 255 + or - 86 mL/min which represents 42% of total acyclovir apparent plasma clearance.
The mechanism of intestinal transport of valacyclovir, the L-valyl ester prodrug of acyclovir, was investigated in rats using an in situ intestinal perfusion technique. Results showed that the oral bioavailability of valacyclovir appears to be significantly influenced by the preabsorptive conversion of valacyclovir to the poorly absorbed acyclovir, by the involvement of multiple transporters in valacyclovir small-intestinal uptake, and by the low permeability of valacyclovir in the colon.
Following oral administration of a 500 mg dose of VALTREX to 5 nursing mothers, peak acyclovir concentrations (Cmax) in breast milk ranged from 0.5 to 2.3 times (median 1.4) the corresponding maternal acyclovir serum concentrations. The acyclovir breast milk AUC ranged from 1.4 to 2.6 times (median 2.2) maternal serum AUC. A 500 mg maternal dosage of VALTREX twice daily would provide a nursing infant with an oral acyclovir dosage of approximately 0.6 mg/kg/day. This would result in less than 2% of the exposure obtained after administration of a standard neonatal dose of 30 mg/kg/day of intravenous acyclovir to the nursing infant. Unchanged valacyclovir was not detected in maternal serum, breast milk, or infant urine.

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Metabolism / Metabolites
Valacyclovir is converted to acyclovir and L-valine via first-pass intestinal and/or hepatic metabolism. Acyclovir is also transformed, to a small extent, to inactive metabolites by _aldehyde oxidase_ in addition to _alcohol dehydrogenase_ and _aldehyde dehydrogenase_. Neither valacyclovir nor acyclovir is metabolized by cytochrome P450 enzymes.
... Aciclovir's main metabolite /is/ 9-carboxymethoxymethylguanine. ...
Valacyclovir is converted to acyclovir and L-valine by first-pass intestinal and/or hepatic metabolism. Acyclovir is converted to a small extent to inactive metabolites by aldehyde oxidase and by alcohol and aldehyde dehydrogenase. Neither valacyclovir nor acyclovir is metabolized by cytochrome P450 enzymes. Plasma concentrations of unconverted valacyclovir are low and transient, generally becoming non-quantifiable by 3 hours after administration. Peak plasma valacyclovir concentrations are generally less than 0.5 ug/mL at all doses. After single-dose administration of 1 gram of Valtrex, average plasma valacyclovir concentrations observed were 0.5, 0.4, and 0.8 ug/mL in patients with hepatic dysfunction, renal insufficiency, and in healthy volunteers who received concomitant cimetidine and probenecid, respectively.

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Biological Half-Life
The plasma elimination half-life of acyclovir typically averaged 2.5 to 3.3 hours in several studies of valacyclovir in volunteers with normal renal function.
The plasma elimination half-life of acyclovir typically averaged 2.5 to 3.3 hours in all studies of Valtrex in volunteers with normal renal function.

Hepatotoxicity
Oral therapy with valacyclovir is associated with a low rate of mild-to-moderate serum aminotransferase elevations, but these abnormalities are usually asymptomatic and self-limited even with continuation of therapy. Complicating the attribution of liver test abnormalities to valacyclovir therapy is the fact that enzyme elevations are not uncommon during the course of varicella-zoster infection (both chickenpox and shingles) and can progress to clinically apparent hepatitis and even acute liver failure. Clinically apparent liver disease due to valacyclovir itself is rare, but isolated reports have been published. The time to onset was short (1 to 2 weeks) and the course mild, with few symptoms and rapid resolution (Case 1). The pattern of liver injury described was mixed hepatocellular-cholestatic. Immunoallergic features and autoantibodies were absent.
Likelihood score: D (possible rare cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
The dosage of acyclovir in milk after valacyclovir is less than 1% of a typical infant dosage and would not be expected to cause any adverse effects in breastfed infants. No special precautions are required when using valacyclovir during breastfeeding. In one study, administration of valacyclovir to mothers with concurrent herpes simplex type 2 and HIV infections reduced breastmilk shedding of the HIV virus in breastmilk at 6 and 14 weeks postpartum, but not later.[1] In another study in HIV-positive mothers, valacyclovir did not reduced breastmilk shedding of cytomegalovirus (CMV) or infant CMV acquisition.[2]
◉ Effects in Breastfed Infants
In a study of pregnant women with concurrent HIV and Herpes simplex infections, mothers received zidovudine 300 mg daily from week of pregnancy until 12 months postpartum and nevirapine at delivery. Half of the women (n = 74) also received valacyclovir 500 mg orally twice daily from 34 weeks gestation until 12 months postpartum. At 6 weeks postpartum, all infants who received acyclovir in breastmilk had normal serum creatinine (<0.83 mg/dL). Their median serum creatinine and alanine aminotransferase (ALT) values, and growth were no different from those of unexposed infants, with the exception of one infant with an ALT level of 70.1 units/L. Infants whose mothers received valacyclovir generally had adverse effects that were similar to the placebo group, except that treated infants had a lower risk of eczema and oral thrush than infants in the placebo arm.[1][4]
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
The binding of valacyclovir to human plasma proteins is low and ranges from 13.5% to 17.9%.

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Interactions
Concomitant use of valacyclovir and probenecid may increase peak plasma concentrations and AUC of acyclovir. This pharmacokinetic interaction is not considered clinically important in patients with normal renal function and no dosage adjustments are necessary in these patients.
Concomitant use of valacyclovir and cimetidine may increase peak plasma concentrations and AUC of acyclovir. This pharmacokinetic interaction is not considered clinically important in patients with normal renal function; no dosage adjustments are necessary in these patients.
Mycophenolate mofetil (MMF) is a drug which decreases the frequency of renal transplantation rejection. However, cytomegalovirus infections are a common feature of this treatment leading the physicians to prescribe antiviral prophylactic drugs like valacyclovir. During this association, neutropenia occur and the cause of this adverse effect is difficult to define. This report presents a case of neutropenia in a woman treated with MMF and valacyclovir. As the duration of the valacyclovir treatment exactly corresponds to the neutropenia duration, and the mycophenolate trough levels increased with the neutrophil count, the responsibility of this neutropenia was ascribed to valacyclovir. However, an examination of the literature for cases of neutropenia led to the suspicion of an interaction between MMF and valacyclovir. Mycophenolate may increase intracellular concentrations of valacyclovir up to hematotoxic levels. This mechanism may explain the interaction and further research is needed to confirm this interaction.

[1]. Valacyclovir. New indication: for genital herpes, simpler administration. Can Fam Physician. 1999 Jul;45:1698-700, 1703-5.

[2]. Acyclovir levels in serum and cerebrospinal fluid after oral administration of valacyclovir. Antimicrob Agents Chemother. 2003 Aug;47(8):2438-41.

[3]. Comparison of efficacies of famciclovir and valaciclovir against herpes simplex virus type 1 in a murineimmunosuppression model. Antimicrob Agents Chemother. 1995 May;39(5):1114-9.

[4]. Dhaliwal DK, Romanowski EG, Yates KA, Valacyclovir inhibits recovery of ocular HSV-1 after experimental reactivation by excimer laser keratectomy. Cornea. 1999 Nov;18(6):693-9.

[5]. Guo A, Hu P, Balimane PV, Interactions of a nonpeptidic drug, valacyclovir, with the human intestinal peptide transporter (hPEPT1) expressed in a mammalian cell line.J Pharmacol Exp Ther. 1999 Apr;289(1):448-54.

Therapeutic Uses
Antiviral Agents
Oral valacyclovir is used in the treatment of initial episodes of genital herpes simplex virus (HSV-2) infection in immunocompetent adults and adolescents. Because many patients with first episodes of genital herpes present with mild clinical symptoms but later develop severe or prolonged symptoms, the US Centers for Disease Control and Prevention (CDC) states that most patients with initial genital herpes should receive antiviral therapy. /Included in US product labeling/
Oral valacyclovir is used in the treatment of recurrent episodes of genital herpes in immunocompetent adults and adolescents. Antiviral therapy for recurrent genital herpes can be given episodically to ameliorate or shorten the duration of lesions or can be given continuously as suppressive therapy to reduce the frequency of recurrences. /Included in US product labeling/
Valacyclovir is used for the episodic treatment of herpes labialis (perioral herpes, cold sores, fever blisters) in adults and adolescents. /Included in US product labeling/
For more Therapeutic Uses (Complete) data for Valacyclovir (9 total), please visit the HSDB record page.

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Drug Warnings
Thrombotic Thrombocytopenic Purpura/Hemolytic Uremic Syndrome (TTP/HUS), in some cases resulting in death, has occurred in patients with advanced HIV-1 disease and also in allogeneic bone marrow transplant and renal transplant recipients participating in clinical trials of Valtrex at doses of 8 grams per day. Treatment with Valtrex should be stopped immediately if clinical signs, symptoms, and laboratory abnormalities consistent with TTP/HUS occur.
There are no adequate and well-controlled studies of Valtrex or acyclovir in pregnant women. Based on prospective pregnancy registry data on 749 pregnancies, the overall rate of birth defects in infants exposed to acyclovir in-utero appears similar to the rate for infants in the general population. Valtrex should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Cases of acute renal failure have been reported in: 1. Elderly patients with or without reduced renal function. Caution should be exercised when administering Valtrex to geriatric patients, and dosage reduction is recommended for those with impaired renal function. 2. Patients with underlying renal disease who received higher than recommended doses of Valtrex for their level of renal function. Dosage reduction is recommended when administering Valtrex to patients with renal impairment. 3. Patients receiving other nephrotoxic drugs. Caution should be exercised when administering Valtrex to patients receiving potentially nephrotoxic drugs. 4. Patients without adequate hydration. Precipitation of acyclovir in renal tubules may occur when the solubility (2.5 mg/mL) is exceeded in the intratubular fluid. Adequate hydration should be maintained for all patients.
The most common adverse reactions reported in at least 1 indication by greater than 10% of adult patients treated with Valtrex and observed more frequently with Valtrex compared to placebo are headache, nausea, and abdominal pain. The only adverse reaction reported in greater than 10% of pediatric patients aged less than 18 years was headache.
For more Drug Warnings (Complete) data for Valacyclovir (8 total), please visit the HSDB record page.

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Pharmacodynamics
**Antiviral effects** Valacyclovir shows varying levels of inhibition towards herpes simplex virus types 1 (HSV-1), 2 (HSV-2), Varicella Zoster Virus (VZV), Epstein-Barr virus (EBV), and cytomegalovirus (CMV). The quantitative relationship between the cell culture susceptibility of herpesviruses to antivirals and the clinical response of humans to the same antiviral therapy has not yet been elucidated. Sensitivity testing results, described by the concentration of drug needed to inhibit the growth of the virus by 50% in cell culture (EC50), vary widely depending on various factors. **Clinical study results** For the various conditions below, clinical study results are summarized as follows: _Cold sores_ Immunocompetent volunteers with cold sores were observed following the administration of a 1-day regimen (2 grams of valacyclovir twice a day for 1 day followed by one day of placebo) or a 2-day regimen (2 grams of valacyclovir twice daily for two days). The average duration of cold sore episodes was approximately 1 day shorter in treated subjects when compared to subjects treated with placebo. A 2-day drug administration regimen of valacyclovir did not provide superior benefit over the 1-day regimen. There was no clinically significant difference observed between subjects receiving valacyclovir or placebo in the prevention of progression of cold sore lesions after the papular stage, indicating that timing of valacyclovir administration is an important consideration. _Initial genital herpes episodes_ 643 immunocompetent adults with first-episode genital herpes who presented within 72 hours of symptom onset were randomized in a double-blind trial to receive 10 days of valacyclovir 1 gram twice daily (n = 323) or oral acyclovir 200 mg 5 times a day (n = 320). In both groups, the median time to healing of herpetic lesions was measured to be 9 days, and the median time to cessation of pain was found to be 5 days, with the median time to cessation of viral shedding was approximately 3 days. _Recurrent genital herpes episodes_ The results of 3 separate studies of patients taking 3 to 5-day regimens of valacyclovir showed an average of 4 days to lesion healing, 2-3 days to resolution of pain associated with the lesions, with an average of 2 days until the cessation of viral shedding. These findings showed valacyclovir administration to show superior beneficial effects when compared to the findings associated with placebo administration. **A note on resistance** The resistance of Herpes Simplex Virus and Varicella Zoster Virus to acyclovir can result from qualitative and quantitative changes in the viral TK and/or DNA polymerase. Clinical isolates of VZV with decreased susceptibility to acyclovir have been isolated from patients diagnosed with AIDS. A total of 522 TK-deficient mutants of VZV have been identified in these cases.

C13H20N6O4

324.341

324.154

C, 48.14; H, 6.22; N, 25.91; O, 19.73

124832-26-4

Valacyclovir hydrochloride;124832-27-5;Valacyclovir hydrochloride hydrate;1218948-84-5

135398742

Typically exists as solid at room temperature

1.5±0.1 g/cm3

170-172

309.7ºC

1.673

-0.88

3

7

8

23

483

1

N[C@@H](C(C)C)C(OCCOCN1C=NC2=C1N=C(N)NC2=O)=O

HDOVUKNUBWVHOX-QMMMGPOBSA-N

InChI=1S/C13H20N6O4/c1-7(2)8(14)12(21)23-4-3-22-6-19-5-16-9-10(19)17-13(15)18-11(9)20/h5,7-8H,3-4,6,14H2,1-2H3,(H3,15,17,18,20)/t8-/m0/s1

2-((2-amino-6-oxo-1,6-dihydro-9H-purin-9-yl)methoxy)ethyl L-valinate

BW-256U87; BW-256; BW256256U87 hydrochloride; BW 256 Val-ACV; Valtrex; Zelitrex; Valacyclovir HCl; Valacyclovir hydrochloride; ValACV; Zelitrex; Valcivir; Valcyclovir; Val-ACV;

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)

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.

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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.)