Enoxaparin (0-70 µg/mL, 90 minutes) amplifies the suppression of hAEc (human airway epithelial cells) caused by HECO-229E infection and the inhibition of TMPRSS2 (transmembrane protease 2) activity by AAT (alpha-1-antitrypsin)[1].

---

Enoxaparin enhances AAT inhibition of TMPRSS2 activity [1]
To determine the effects of UFH, Enoxaparin, or nadroparin, the cells were left untreated or pre-incubated for 30 min with AAT alone at 1 and 3 mg/mL, or with combined 3 mg/mL AAT with two different concentrations of UFH, nadroparin, or enoxaparin. UFH at both concentrations elicited a modest further reduction of TMPRSS2 activity compared with AAT 3 mg/mL alone, particularly at the longer incubation times (Fig. 3A), whereas nadroparin did not (Fig. 3B). In contrast, enoxaparin + AAT most potently inhibited TMPRSS2 activity in a dose-dependent manner compared with AAT alone (Fig. 3C,D). Because the HEK293TTMPRSS2 cells were pre-treated with both AAT and enoxaparin for 30 min, it is not unexpected that there would be decreased TMPRSS2 activity from the onset of the assay.

We next determined whether the heparins alone also inhibited TMPRSS2. Unexpectedly, we found that UFH alone had a modest dose–response inhibitory effect on TMPRSS2 activity (Fig. 4A). Nadroparin had minimal impact and only at higher nadroparin concentrations at the longer time points (Fig. 4B). Enoxaparin alone at 35 and 70 µg/mL significantly inhibited TMPRSS2 activity at the 90 min incubation period (Fig. 4C). Because the experiments were performed in cell culture medium that includes fetal bovine serum that is likely to contain native AAT (and perhaps other serpins), we performed the experiments with enoxaparin alone in Gibco 293 Serum-free Medium II. In the absence of serum, enoxaparin had little or no inhibitory effect on TMPRSS2 activity (Fig. 4D).

---

Enoxaparin augments AAT inhibition of HCoV-229E infection of primary human airway epithelial cells [1]
To determine the effects of AAT, Enoxaparin, or both on coronavirus infection, we quantified viral load by immunofluorescent staining for the nucleocapsid protein and by the plaque assay of primary human airway epithelial cells (hAEc) cultured in air–liquid interface infected with the human coronavirus 229E (HCoV-229E). Compared with no infection, cells infected with HCoV-229E immunostained positively for the viral nucleoprotein (Fig. 5A,B). Pre-treatment of hAEc with AAT, enoxaparin, or both, reduced the number of cells that stained positive for the nucleoprotein.

The burden of HCoV-229E was also quantified by the plaque assay in which the supernatant from the apical chambers of the uninfected and infected hAEc in air–liquid interface were used to infect VeroE6 cells. Incubation of the VeroE6 cells with 10–7 dilution of the supernatant of HCoV-229E-infected hAEc demonstrated visually quantifiable plaques (Fig. 5C). In VeroE6 cells incubated with medium from HCoV-229E-infected hAEc treated with AAT, there was a modest but significant reduction in the number of plaques and a further decrease with both AAT and Enoxaparin. Interestingly, there was also a modest but consistent decrease in the number of plaques with enoxaparin alone.

Enoxaparin (1 mg/kg; SC; every 6 hours for 8 doses) decreases oxidative damage, inflammation, and astrocytosis following TBI (traumatic brain injury) in rats [2].

---

Purpose of this study was to investigate the effects of low molecular weight heparin, Enoxaparin, on different parameters of the hippocampal damage following traumatic brain injury (TBI) in the rat. TBI of moderate severity was performed over the left parietal cortex using the lateral fluid percussion brain injury model. Animals were s.c. injected with either enoxaparin (1mg/kg) or vehicle 1, 7, 13, 19, 25, 31, 37, and 43 h after the TBI induction. Sham-operated, vehicle-treated animals were used as the control group. Rats were sacrificed 48h after the induction of TBI. Hippocampi were processed for spectrophotometric measurements of the products of oxidative lipid damage, thiobarbituric acid-reactive substances (TBARS) levels, as well as the activities of antioxidant enzymes, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). Moreover, the Western blotting analyses of the oxidized protein levels, expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), pro- and mature-interleukin-1β (pro-, and mature-IL-1β), and active caspase-3 were performed. COX-2 expressions were also explored by using immunohistochemistry. Glial fibrillary acidic protein immunochistochemistry was performed with the aim to assess the level of astrocytic activity. Fluoro-Jade B staining was used to identify the level and extent of hippocampal neuronal injury. TBI caused statistically significant increases of the hippocampal TBARS and oxidized protein levels as well as COX-2, pro-IL-1β, and active caspase-3 overexpressions, but it did not significantly affect the SOD and GSH-Px activities, the iNOS, and mature-IL-1β expression levels. TBI also induced hippocampal reactive astrocytosis and neurodegeneration. Enoxaparin significantly decreased the hippocampal TBARS and oxidized protein levels, COX-2 overexpression and reactive gliosis, but it did not influence the SOD and GSH-Px activities, pro-IL-1β and active caspase-3 overexpressions as well as neurodegeneration following TBI. These findings demonstrate that enoxaparin may reduce oxidative damage, inflammation and astrocytosis following TBI in the rat and could be a candidate drug for neuroprotective treatment of this injury. [2]

---

Enoxaparin is a low-molecular-weight heparin (LMWH) derivative that exerts its anticoagulant activity through antithrombin III, an endogenous inhibitor of factor Xa and thrombin IIa. Unlike its unfractionated heparin (UFH) counterparts, Enoxaparin has a greater bioavailability, lower incidence of heparin-induced thrombocytopenia and more stable and predictable anticoagulation, allowing fixed dosing without the need for monitoring. These advantages make it an attractive anticoagulant to be used in acute coronary syndrome management. Indeed, several clinical trials and meta-analyses have consistently demonstrated the efficacy of enoxaparin in reducing cardiovascular events and mortality in this population. Although initial clinical trials with enoxaparin during the early conservative approach suggested superior efficacy without differences in safety compared with UFH, emerging data in the current era of early revascularization approach indicate that superior effects of enoxaparin over heparin in reducing clinical events should be balanced against an increase in major hemorrhagic complications. Enoxaparin is a rational alternative to UFH in patients presenting with either unstable angina/non-ST-elevation myocardial infarction or ST-elevation myocardial infarction, with a clinically modest increase in bleeding complications [3].

Measurement of TMPRSS2 activity [1]
HEK293T cells that overexpress TMPRSS2 (HEK293TTMPRSS2) were left untreated or pre-treated with AAT (1, 3, and 5 mg/mL), UFH (1.5 and 8 U/mL), Enoxaparin (35 and 70 μg/mL), nadroparin (2.2 and 8.8 U/mL), and/or AEBSF (50 μM) and incubated at 25 °C for 30 min, followed by the addition of 100 µM of the fluorogenic substrate Boc-QAR-AMC. Fluorescence was immediately measured using a UV filter (excitation 365 nm and emission 410 nm) and then every 15 min for a total of 90 min at 37 °C in a SpectraMax M2e Microplate Reader and reported as arbitrary fluorescent units (AFU).

---

Infection of hAEc with human coronavirus 229E [1]
After culture and differentiation of hAEc grown on ALI for 3–4 weeks, the medium was replaced with fresh medium alone or pre-treated for 1 h with medium containing AAT (3 mg/mL), Enoxaparin (70 μg/mL), or both in both the apical and bottom chambers of the 24-well Transwell plate, followed by infection with human coronavirus 229E (HCoV-229E) at an multiplicity-of-infection of 1 hAEc:0.01 HCoV-229E in the apical chamber. HCoV-229E is an instructive viral challenge because the virus also uses TMPRSS2 to process its spike protein. Unlike other less virulent human coronaviruses, HCoV-229E has been associated with respiratory failure manifested as the acute respiratory distress syndrome64. In addition, since our focus was to study the effects of AAT on viral infection in the context of AAT inhibition of TMPRSS2, we utilized a coronavirus which uses a different receptor (aminopeptidase N rather than ACE2) since AAT has been shown to inhibit ADAM17, which induces shedding of ACE2 from the cell surface. After two hours of incubation for viral adsorption, the cells in the apical chamber were washed with wash buffer (PBS:medium 1:1). After incubation at 37 °C (5% CO2) for 3 days, 150 μL of the medium was added to each apical chamber, incubated for 30 min, and the supernatant in the apical chamber was pipetted gently to recover the viral particles. The hAEc seeded on the transwells were also saved for viral protein immunostaining. All samples were stored at − 80 °C until assayed.

Cell Viability Assay[1]
Cell Types: HEK293T TMPRSS2 cells, hAEc
Tested Concentrations: 0, 8.8, 35, 70 µg/mL
Incubation Duration: 90 min
Experimental Results: Significant inhibition of TMPRSS2 during 90 min incubation period at 35 and 70 µg/mL activity, enhance AAT's inhibition of TMPRSS2 activity, and enhance AAT's inhibition of HCoV-229E infection of hAEc.

Animal/Disease Models: Adult male Wistar rat (350-450 g, treated with TBI) [2]
Doses: 0 mg/kg, 1 mg/kg
Route of Administration: subcutaneous injection, once every 6 hrs (hrs (hours)), starting at 1 hour, to 43 hrs (hrs (hours)) after completion of TBI induction.
Experimental Results: Dramatically diminished hippocampal TBARS and oxidative protein levels, COX-2 overexpression and reactive gliosis, but did not affect SOD and GSH-Px activity, pro-IL-1β and active caspase-3 overexpression and after TBI of neurodegeneration. Reduce oxidative damage, inflammation, and astrocytosis after TBI in rats.

---

Experiments were performed on adult male Wistar rats weighing from 350 to 450 g. Rats were maintained on a 12 h light–dark cycle and allowed free access to food and water. All experiments were performed between 10 am and 2 pm in a silent room, at a temperature of 22 °C–24 °C. Faculty ethical committee approved all experimental procedures involving animals, which were carried out in accordance with the related Croatian laws and rules (NN 19/99; NN 176/04) and with the guidelines set by the European Community Council Directive of 24 November 1986 (86/609/EEC).
TBI was induced using the LFPI mode. Rats were anesthetized with isoflurane (4% induction, 2% maintenance) and fixed in a stereotaxic frame. A 5 mm craniotomy was made over the left parietal cortex (3.4 mm lateral to midline and midway between bregma and lambda sutures), leaving the dura intact. A hollow female Luer Lock fitting was positioned over the craniotomy and held in place with dental cement. Animals were attached to the fluid percussion injury device (VCU Biomedical Engineering Facility, Richmond, VA, USA) via the Luer-Lock fitting and brain injury of moderate severity (1.8–2.2 atm) was induced. The magnitude of the pressure pulse, approximately 20 ms in duration, was software controlled i.e. measured by a pressure transducer and recorded on a digital storage oscilloscope. Animal apnea time after the injury was measured and only the rats with apnea duration less than 60 s were included in the analyses. After finishing the surgical procedures, animals were returned to their home cages with food and water available ad libitum. During the surgical procedures and recovery, animals' body temperature was monitored with a rectal thermometer and maintained at 37 °C.
Animals were randomly divided into three experimental groups (n = 17 per group). Rats of the control group were sham-operated, vehicle treated. They were handled identically to the TBI-treated rats but were not subjected to the brain injury. TBI was performed on the rats of two other groups which were s.c. injected with 1 mg/kg Enoxaparin or vehicle every 6 h, starting at 1 h, and finishing at 43 h after the TBI induction. [2]

Absorption, Distribution and Excretion
Pharmacokinetic trials were conducted using the 100 mg/mL formulation. Maximum anti-Factor Xa and anti-thrombin (anti-Factor IIa) activities occur 3 to 5 hours after SC injection of enoxaparin. Mean peak anti-Factor Xa activity was 0.16 IU/mL (1.58 mcg/mL) and 0.38 IU/mL (3.83 mcg/mL) after the 20 mg and the 40 mg clinically tested SC doses, respectively. Mean (n = 46) peak anti-Factor Xa activity was 1.1 IU/mL at steady state in patients with unstable angina receiving 1 mg/kg SC every 12 hours for 14 days. Mean absolute bioavailability of enoxaparin, after 1.5 mg/kg given SC, based on anti-Factor Xa activity is approximately 100% in healthy subjects.
A 30 mg IV bolus immediately followed by a 1 mg/kg SC every 12 hours provided initial peak anti-Factor Xa levels of 1.16 IU/mL (n=16) and average exposure corresponding to 84% of steady-state levels. Steady state is achieved on the second day of treatment.
Enoxaparin pharmacokinetics appear to be linear over the recommended dosage ranges. After repeated subcutaneous administration of 40 mg once daily and 1.5 mg/kg once-daily regimens in healthy volunteers, the steady state is reached on day 2 with an average exposure ratio about 15% higher than after a single dose. Steady-state enoxaparin activity levels are well predicted by single-dose pharmacokinetics. After repeated subcutaneous administration of the 1 mg/kg twice daily regimen, the steady state is reached from day 4 with mean exposure about 65% higher than after a single dose and mean peak and trough levels of about 1.2 and 0.52 IU/mL, respectively. Based on enoxaparin sodium pharmacokinetics, this difference in steady state is expected and within the therapeutic range.
The volume of distribution of anti-Factor Xa activity is about 4.3 L.
For more Absorption, Distribution and Excretion (Complete) data for Enoxaparin sodium (16 total), please visit the HSDB record page.

---

Metabolism / Metabolites
Enoxaparin sodium is primarily metabolized in the liver by desulfation and/or depolymerization to lower molecular weight species with much reduced biological potency. Renal clearance of active fragments represents about 10% of the administered dose and total renal excretion of active and non-active fragments 40% of the dose.

---

Biological Half-Life
Elimination half-life based on anti-Factor Xa activity was 4.5 hours after a single SC dose to about 7 hours after repeated dosing.

[1]. Enoxaparin augments alpha-1-antitrypsin inhibition of TMPRSS2, a promising drug combination against COVID-19. Sci Rep. 2022 Mar 25;12(1):5207.

[2]. Effects of enoxaparin in the rat hippocampus following traumatic brain injury. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Dec 1;35(8):1846-56.

[3]. Lee S, Gibson CM. Enoxaparin in acute coronary syndromes. Expert Rev Cardiovasc Ther. 2007 May;5(3):387-99.

Enoxaparin Sodium is the sodium salt of enoxaparin, a low molecular weight, synthetic heparin. As an anticoagulant/antithrombotic agent, enoxaprin's mechanism of action is similar to that of heparin, although it exhibits a higher ratio of anti-Factor Xa to anti-Factor IIa activity. This agent also has anti-inflammatory properties, inhibiting monocyte adhesion to tumor necrosis factor alpha- or lipopolysaccharide-activated endothelial cells. Compared to unfractionated heparins, the use of enoxaparin is associated with lower incidences of osteoporosis and heparin-induced thrombocytopenia.

---

Drug Indication
Inhixa is indicated for adults for: Prophylaxis of venous thromboembolism, particularly in patients undergoing orthopaedic, general or oncological surgery. Prophylaxis of venous thromboembolism in patients bedridden due to acute illnesses including acute heart failure, acute respiratory failure, severe infections, as well as exacerbation of rheumatic diseases causing immobilisation of the patient (applies to strengths of 40 mg/0. 4 mL). Treatment of deep vein thrombosis (DVT), complicated or uncomplicated by pulmonary embolism. Treatment of unstable angina and non Q wave myocardial infarction, in combination with acetylsalicylic acid (ASA). Treatment of acute ST segment elevation myocardial infarction (STEMI) including patients who will be treated conservatively or who will later undergo percutaneous coronary angioplasty (applies to strengths of 60 mg/0. 6 mL, 80 mg/0. 8 mL, and 100 mg/1 mL). Blood clot prevention in the extracorporeal circulation during haemodialysis.
Thorinane is indicated for adults for: , , - Prophylaxis of venous thromboembolism, particularly in patients undergoing orthopaedic, general or oncological surgery. , , - Prophylaxis of venous thromboembolism in patients bedridden due to acute illnesses including acute heart failure, acute respiratory failure, severe infections, as well as exacerbation of rheumatic diseases causing immobilisation of the patient (applies to strengths of 40 mg/0. 4 mL). , , - Treatment of deep vein thrombosis (DVT), complicated or uncomplicated by pulmonary embolism. , , - Treatment of unstable angina and non Q wave myocardial infarction, in combination with acetylsalicylic acid (ASA). , , - Treatment of acute ST segment elevation myocardial infarction (STEMI) including patients who will be treated conservatively or who will later undergo percutaneous coronary angioplasty (applies to strengths of 60 mg/0. 6 mL, 80 mg/0. 8 mL, and 100 mg/1 mL). , , - Blood clot prevention in the extracorporeal circulation during haemodialysis. , , Prevention and treatment of various disorders related to blood clots in adults. ,

---

Mechanism of Action
Enoxaparin is a low molecular weight heparin which has antithrombotic properties.
Enoxaparin has an approximate anti-factor Xa activity of 100 units/mg according to the World Health Organization (WHO) First International Low Molecular Weight Heparin Reference Standard. At a given level of anti-factor Xa activity, enoxaparin has less effect on thrombin than does unfractionated heparin. However, enoxaparin administration has been associated with a prolongation of some global clotting function tests (ie, thrombin time, activated partial thromboplastin time [aPTT]) by up to 1.8 times the control value.
In humans, enoxaparin given at a dose of 1.5 mg/kg subcutaneously (SC) is characterized by a higher ratio of anti-Factor Xa to anti-Factor IIa activity (mean +/- SD, 14.0 +/- 3.1) (based on areas under anti-Factor activity versus time curves) compared to the ratios observed for heparin (mean +/- SD, 1.22 +/- 0.13). Increases of up to 1.8 times the control values were seen in the thrombin time (TT) and the activated partial thromboplastin time (aPTT). Enoxaparin at a 1 mg/kg dose (100 mg / mL concentration), administered SC every 12 hours to patients in a large clinical trial resulted in aPTT values of 45 seconds or less in the majority of patients (n = 1607). A 30 mg IV bolus immediately followed by a 1 mg/kg SC administration resulted in aPTT post-injection values of 50 seconds. The average aPTT prolongation value on Day 1 was about 16% higher than on Day 4.

C42H59N3NA4O35S2

1322.00

1321.196

679809-58-6

60196282

White to off-white solid powder

13

36

17

86

2530

24

S(NC1C2OCC(C(C1O)OC1C(C(C(C(C(=O)[O-])O1)OC1C(C(C)C(C(CO)O1)OC1CC(C(=O)[O-])C(C(C1O)O)OC1C(C(C(C(COS(=O)(=O)O)O1)OC1C(C(C=C(C(=O)[O-])O1)O)O)O)NC(C)=O)NC(C)=O)O)O)O2)(=O)(=O)[O-].[Na+].[Na+].[Na+].[Na+]

CIJQTPFWFXOSEO-NDMITSJXSA-J

InChI=1S/C42H63N3O35S2.4Na/c1-9-19(43-10(2)47)39(79-33-27(55)28(56)42(80-34(33)37(61)62)78-31-17-7-69-38(74-17)21(25(31)53)45-81(63,64)65)73-16(6-46)29(9)71-14-4-12(35(57)58)30(26(54)23(14)51)76-40-20(44-11(3)48)24(52)32(18(75-40)8-70-82(66,67)68)77-41-22(50)13(49)5-15(72-41)36(59)60;;;;/h5,9,12-14,16-34,38-42,45-46,49-56H,4,6-8H2,1-3H3,(H,43,47)(H,44,48)(H,57,58)(H,59,60)(H,61,62)(H,63,64,65)(H,66,67,68);;;;/q;4*+1/p-4/t9-,12?,13+,14-,16-,17-,18-,19-,20-,21-,22-,23+,24-,25-,26-,27-,28-,29+,30-,31?,32-,33?,34?,38-,39-,40-,41+,42-;;;;/m1..../s1

tetrasodium;(2R,3R,4S)-2-[(2R,3S,4R,5R,6S)-5-acetamido-6-[(1R,2R,3R,4R)-4-[(2R,3S,4R,5R,6R)-5-acetamido-6-[(4R,5R,6R)-2-carboxylato-4,5-dihydroxy-6-[[(1R,3R,4R,5R)-3-hydroxy-4-(sulfonatoamino)-6,8-dioxabicyclo[3.2.1]octan-2-yl]oxy]oxan-3-yl]oxy-2-(hydroxymethyl)-4-methyloxan-3-yl]oxy-6-carboxylato-2,3-dihydroxycyclohexyl]oxy-4-hydroxy-2-(sulfooxymethyl)oxan-3-yl]oxy-3,4-dihydroxy-3,4-dihydro-2H-pyran-6-carboxylate

Enoxaparin sodium; ENOXAPARIN SODIUM, EP STANDARD; Monomer of enoxaparin sodium; DTXSID00872764; DSSTox_CID_25969; .

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)

H2O : ≥ 100 mg/mL

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.)