- Branched-chain alpha-keto acid dehydrogenase kinase (BCKDK) - Octanoic acid inhibits hepatic BCKDK (a negative regulator of branched-chain alpha-keto acid dehydrogenase, BCKDH), but no specific IC50 or Ki values were reported [3]
- Olfactory receptor 51E2 (OR51E2) - Octanoic acid binds to OR51E2 in pancreatic β-cells to modulate insulin secretion, with no measured binding affinity (KD) or EC50 values provided [4]

- Neurotrophic effects (PC12 cells):
1. Neurite outgrowth promotion: Octanoic acid (100–400 μM) treatment for 72 hours increased neurite length by 2.0–3.5-fold and neurite-bearing cell ratio by 40–60% in PC12 cells (compared to vehicle control). At 200 μM, it induced maximal neurite outgrowth, comparable to nerve growth factor (NGF, 50 ng/mL) [5]
2. Signaling activation: Octanoic acid (100–400 μM) increased phosphorylation of ERK1/2 (1.5–2.5-fold) and Akt (1.2–1.8-fold) in PC12 cells, as detected by western blot. Inhibition of ERK pathway (U0126, 10 μM) abolished neurite outgrowth induced by octanoic acid [5]
- Insulin secretion modulation (pancreatic β-cells):
1. Glucose-stimulated insulin secretion (GSIS) enhancement: In INS-1 rat insulinoma cells, octanoic acid (100–500 μM) potentiated GSIS (16.7 mM glucose) by 1.5–2.2-fold. This effect was abolished by OR51E2 siRNA transfection, indicating OR51E2 dependence [4]
2. Glucokinase (GK) upregulation: octanoic acid (200 μM) increased GK mRNA expression by 1.8-fold and GK protein levels by 1.6-fold in INS-1 cells (qPCR and western blot analysis) [4]
- Branched-chain amino acid (BCAA) catabolism regulation (primary hepatocytes):
1. BCKDH activation: Octanoic acid (100–500 μM) treatment for 4 hours increased hepatic BCKDH activity by 1.3–2.0-fold in rat primary hepatocytes. This was associated with reduced BCKDK protein levels (by 30–50%) [3]
2. BCAA degradation promotion: Octanoic acid (300 μM) increased the degradation rate of [14C]-labeled leucine (a BCAA) by 40% in primary hepatocytes [3]

- Tremor suppression (essential tremor mouse model):
1. Harmaline-induced tremor attenuation: Male ICR mice (25–30 g) received octanoic acid (100 or 200 mg/kg, ip) 30 minutes before harmaline (50 mg/kg, ip). At 200 mg/kg, octanoic acid reduced tremor score (0–3 scale) from 2.8 (vehicle) to 1.2 and decreased tremor frequency (Hz) by 35% (measured by accelerometer and visual scoring) [1]
2. Duration of effect: The tremor-suppressive effect lasted for 2–3 hours post-administration [1]
- Parkinson’s disease protection (MPTP mouse model):
1. Dopamine preservation: Male C57BL/6 mice (20–25 g) received octanoic acid (100 mg/kg, ip) daily for 5 days, with MPTP (20 mg/kg, ip) administered on days 2–4. Octanoic acid prevented MPTP-induced striatal dopamine (DA) reduction: DA levels were 85% of control (vs. 40% in MPTP-only group) as measured by HPLC [2]
2. Motor function improvement: Octanoic acid reversed MPTP-induced deficits in rotarod performance (latency to fall increased from 40 s to 80 s) and open-field locomotor activity (distance traveled increased by 50%) [2]
- BCAA metabolism regulation (rat model):
1. Plasma BCAA reduction: Male Sprague-Dawley rats (250–300 g) were orally administered octanoic acid (200 or 400 mg/kg) daily for 7 days. At 400 mg/kg, plasma leucine, isoleucine, and valine concentrations decreased by 30%, 25%, and 28%, respectively [3]
2. Hepatic BCKDH activation: Octanoic acid (400 mg/kg, oral) increased hepatic BCKDH activity by 60% and reduced hepatic BCKDK protein levels by 45% in rats [3]

- BCKDK inhibition assay (rat liver) [3]:
1. Enzyme extraction: Rat liver tissue was homogenized in lysis buffer (20 mM Tris-HCl, pH 7.5, 150 mM NaCl, 1 mM EDTA, 1% Triton X-100) and centrifuged at 12,000×g for 20 minutes to obtain BCKDK-containing supernatant.
2. Reaction setup: The assay mixture (200 μL) contained BCKDK extract (50 μg protein), BCKDH substrate (100 μM branched-chain alpha-keto acids), ATP (1 mM), MgCl2 (5 mM), and octanoic acid (0.1–1 mM, vehicle: ethanol).
3. Activity measurement: BCKDH activity (indicator of BCKDK inhibition) was measured by monitoring NADH production at 340 nm for 30 minutes. Relative activity was calculated compared to the vehicle control.
- Insulin secretion assay (INS-1 cells) [4]:
1. Cell preparation: INS-1 cells were cultured in RPMI 1640 medium with 10% FBS and synchronized in glucose-free Krebs-Ringer bicarbonate buffer (KRBB) for 2 hours.
2. Stimulation and detection: Cells were treated with octanoic acid (100–500 μM) in KRBB containing 2.8 mM (low glucose) or 16.7 mM (high glucose) glucose for 1 hour. Insulin in the supernatant was quantified by ELISA, and GSIS was calculated as the ratio of insulin secretion under high vs. low glucose.

- PC12 cell neurite outgrowth assay [5]:
1. Cell culture: PC12 cells were seeded in 24-well plates (5×10⁴ cells/well) in DMEM with 10% FBS and 5% horse serum.
2. Drug treatment: After 24 hours, octanoic acid (100–400 μM, vehicle: ethanol) or NGF (50 ng/mL, positive control) was added, and cells were cultured for 72 hours.
3. Neurite quantification: Cells were fixed with 4% paraformaldehyde, stained with crystal violet, and observed under a light microscope. Neurite length and neurite-bearing cells were counted in 5 random fields per well; neurites longer than twice the cell body diameter were considered positive.
4. Signaling detection: For western blot, PC12 cells were lysed in RIPA buffer, and proteins (30 μg) were probed with anti-p-ERK1/2, anti-ERK1/2, anti-p-Akt, and anti-Akt antibodies.
- Primary hepatocyte BCKDH activity assay [3]:
1. Hepatocyte isolation: Rat primary hepatocytes were isolated by collagenase perfusion and seeded in 6-well plates (1×10⁶ cells/well) in William’s E medium.
2. Drug treatment: Octanoic acid (100–500 μM) was added 24 hours post-seeding, and cells were incubated for 4 hours.
3. BCKDH activity measurement: Cells were homogenized, and BCKDH activity was assayed by monitoring NADH production at 340 nm after adding branched-chain alpha-keto acids and cofactors.

- Mouse essential tremor model [1]:
1. Animal selection: Male ICR mice (25–30 g) were acclimated for 7 days before experimentation.
2. Drug formulation: Octanoic acid was dissolved in physiological saline (pH adjusted to 7.4 with NaOH) to concentrations of 10 mg/mL (100 mg/kg dose) and 20 mg/mL (200 mg/kg dose).
3. Administration: Mice received intraperitoneal (ip) injections of octanoic acid (10 mL/kg volume) 30 minutes before ip injection of harmaline (5 mg/mL in saline, 50 mg/kg).
4. Tremor assessment: Tremor was evaluated visually (score 0–3: 0=no tremor, 3=severe tremor) and by accelerometer (recording frequency and amplitude) at 15, 30, 60, 90, 120, and 180 minutes post-harmaline injection.
- Mouse MPTP Parkinson’s model [2]:
1. Animal selection: Male C57BL/6 mice (20–25 g) were used.
2. Drug formulation: Octanoic acid was dissolved in saline (pH 7.4) to 10 mg/mL.
3. Administration schedule: Mice received daily ip injections of octanoic acid (100 mg/kg, 10 mL/kg) on days 1–5. MPTP (2 mg/mL in saline) was administered ip at 20 mg/kg on days 2–4 (once daily).
4. Endpoint measurements: On day 6, mice were euthanized; striatum was dissected for dopamine analysis (HPLC). Motor function was assessed by rotarod test (5 rpm acceleration) and open-field test (5-minute session) on day 5.
- Rat BCAA metabolism model [3]:
1. Animal selection: Male Sprague-Dawley rats (250–300 g) were fasted overnight before experimentation.
2. Drug formulation: Octanoic acid was dissolved in corn oil to concentrations of 20 mg/mL (200 mg/kg dose) and 40 mg/mL (400 mg/kg dose).
3. Administration: Rats received oral gavage of octanoic acid (10 mL/kg volume) daily for 7 days. Control rats received corn oil alone.
4. Endpoint measurements: On day 8, blood was collected via cardiac puncture for plasma BCAA analysis (HPLC); liver tissue was harvested for BCKDH activity assay and BCKDK western blot.

Absorption, Distribution and Excretion
For children with epilepsy whose condition is uncontrolled by medication, the medium-chain triglyceride (MCT) diet appears to have been successful. The MCT diet is an emulsion whose main component (81%) is caprylic acid, and it also contains 15% decanoic acid. In this study, 15 children obtained 50% to 60% of their energy requirements from the MCT emulsion. Researchers analyzed the levels of decanoic acid and caprylic acid in blood samples. There were significant differences in absolute levels, possibly due to poor patient compliance, but all patients had lower levels in the morning and higher levels in the evening. This suggests that both acids are rapidly metabolized. /Medium-chain Triglycerides/ To assess the in vivo distribution kinetics of selected valproic acid structural analogues, this study investigated the pharmacokinetics of valproic acid and its three structural analogues—cyclohexanecarboxylic acid, 1-methyl-1-cyclohexanecarboxylic acid (1-methylcyclohexanecarboxylic acid), and caprylic acid—in female rats. All four carboxylic acids showed dose-dependent distribution. Systemic clearance of each compound decreased with increasing dose, suggesting a saturable clearance process. Except for cyclohexanecarboxylic acid, the apparent volume of distribution of these compounds was dose-dependent, indicating that their binding to proteins in serum and/or tissues may be saturable. Valproic acid and 1-methylcyclohexanecarboxylic acid both exhibited enterohepatic circulation, and this circulation appeared to be dose- and compound-specific. Valproic acid and 1-methylcyclohexanecarboxylic acid were excreted in large quantities in the urine. Octanoic acid and cyclohexanecarboxylic acid were not excreted in the urine, and no enterohepatic circulation was observed. This leads to the conclusion that small changes in the chemical structure of low molecular weight carboxylic acids can affect their metabolism and distribution.
Metabolism/Metabolites

After administration of octanoic acid to rats, it is rapidly metabolized in the liver and many other tissues, generating carbon dioxide and two-carbon fragments that integrate into long-chain fatty acids and other water-soluble products.
Medium-chain acyl-CoA dehydrogenase (MCAD) is responsible for the dehydrogenation step in the β-oxidation of fatty acids with 6 to 12 carbon atoms in mitochondria. Fatty acid β-oxidation provides energy after the body's glucose and glycogen reserves are depleted. This typically occurs during prolonged fasting or illness, when calorie intake is reduced and energy demand increases. β-oxidation of long-chain fatty acids produces two carbon units: acetyl-CoA and reducing equivalents NADH and FADH2. NADH and FADH2 enter the electron transport chain to synthesize ATP. Acetyl-CoA enters the tricarboxylic acid cycle and also synthesizes ATP via electron transport and substrate-level phosphorylation. When the supply of acetyl-CoA (from fatty acid β-oxidation) exceeds the tricarboxylic acid cycle's ability to metabolize acetyl-CoA, excess acetyl-CoA molecules are converted into ketone bodies (acetoacetic acid and β-hydroxybutyrate) by HMG-CoA synthase in the liver. Ketone bodies can also be used as energy, particularly for the brain and heart; in fact, after the third day of fasting, ketone bodies become the primary energy source for these two organs. (Wikipedia) - Oral absorption (rat): After oral administration of caprylic acid (400 mg/kg, dissolved in corn oil), the peak plasma concentration (Cmax) is 150–200 μM, and the time to peak concentration is 1–2 hours (Tmax). The oral bioavailability is approximately 85–90% [3] - Distribution: In rats, caprylic acid is preferentially distributed in the liver (tissue/plasma concentration ratio: 2.5–3.0) and pancreas (1.8–2.0). It can cross the blood-brain barrier, and the concentration in brain tissue can reach 30–40% of the plasma concentration [2,3] - Metabolism and excretion: Caprylic acid is rapidly metabolized in the liver to acetyl-CoA (a substrate of the tricarboxylic acid cycle) via β-oxidation. Approximately 90% of the administered dose is oxidized to CO2 and excreted by respiration within 24 hours; <5% is excreted unchanged in the urine. [3]
- Elimination half-life: The plasma elimination half-life (t1/2) of caprylic acid in rats was 1.5–2.0 hours [3]

Toxicity Summary
Cosmetic Ingredient Review Conclusion
The CIR expert panel concluded that the following ingredient is safe when formulated as non-irritating and non-sensitizing at the current methods of use and concentrations described in the safety assessment, possibly based on a quantitative risk assessment (QRA)... Sodium caprylate...

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Non-human Toxicity Excerpt
In rabbits, intravenous administration of sodium caprylate resulted in a significant but transient inhibition of platelet reactivity, as measured by laser technology. A single oral dose of sodium caprylate had no effect on platelet adhesion. Long-term (2 and 3 weeks) oral administration resulted in a gradual and significant decrease in platelet adhesion in rabbits. Other hematological parameters, such as hematocrit, plasma cholesterol, triglycerides, and ketone body concentrations, were not affected by treatment. TANGEN O et al.; Nordic Journal of Clinical Laboratory Research 35(1) 19 (1975)
Inducing sodium caprylate (5 mmol/kg) in rhesus monkeys (Macaca mulatta) resulted in 20 minutes of coma with myoclonus, followed by complete loss of muscle tone and loss of eye movement. STAEFFEN J et al.; CR SOC BIOL 167(11) 1595 (1974)
Intravenous injection of sodium caprylate at a dose of 5 mmol/kg over 20 minutes produced a clinical and EEG syndrome similar to hepatic encephalopathy in 5 rhesus monkeys (Macaca mulatta). RABINOWITZ JL et al.; AM J GASTROENTEROL 69(2) 187 (1978)
0.2 mol sodium caprylate solution was administered to rabbits by continuous slow intravenous infusion over 4 hours. Significant regional (sodium, potassium)-ATPase activity inhibition was detected in the cortex, thalamus, hypothalamus, pons, and medulla oblongata. TRAUNER DA; PEDIATR RES 14(6) 844 (1980)

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Toxicity Overview
Caprylic acid (OA) and capric acid (DA) have been shown to impair the function of glycolysis and the citric acid cycle, increase hepatic oxygen consumption, and inhibit certain activities of respiratory chain complexes and creatine kinase in the rat brain (A15454, A15455). These fatty acids have also been shown to induce oxidative stress in the brain (A15456). Experiments have shown that OA and DA impair mitochondrial energy homeostasis in the brain, which may be at least partly the basis of the neuropathology of MCADD (A15457).

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Toxicity Data
Oral LD₅₀ in rats: 10080 mg/kg. Intravenous LD₅₀ in mice: 600 mg/kg. Rabbit skin LD50: Over 5000 mg/kg. Interactions This study investigated the duration of the absorption-enhancing effects of sodium caprylate (C8), sodium hexanoate (C6), and glycerol-L-monocaprylate (MO) on rectal absorption of gentamicin via empty suppositories in rabbits. To assess the duration of the absorption-enhancing effect of pretreatment (administration of an absorption enhancer before gentamicin administration), suppository I containing each absorption enhancer was placed rectally. Then, suppository II containing gentamicin was administered at predetermined time points (i.e., 10, 33, 2, 6, and 24 hours after administration of suppository I). Plasma gentamicin concentrations in the absorption enhancer pretreatment group were compared with those in the group receiving both gentamicin and the absorption enhancer. Pretreatment with C8, C6, or glycerol-L-monocaprylate 16 and 24 hours prior to rectal administration of gentamicin significantly reduced the AUC and Cmax of gentamicin compared to simultaneous administration of gentamicin and C8, C6, or glycerol-L-monocaprylate. The facilitating effect of C8, C6, and glycerol-L-monocaprylate on rectal gentamicin absorption was significantly reduced by prolonging the time interval between pretreatment with each absorption enhancer and gentamicin administration. The absorption-enhancing effect of C6 was shorter in duration than that of C8, while the duration of glycerol-L-monocaprylate was similar to that of C8. The effects of these absorption enhancers disappeared 24 hours after pretreatment. These results indicate that the reduction in membrane transport barrier function recovers approximately one day after administration of C8 or MO.
The activity of cytochrome oxidase in choroid plexus epithelial cells was investigated using histochemical methods. Strong staining of this enzyme was limited to mitochondria. Caprylate-treated rat choroid plexus epithelial cells exhibited extensive ultrastructural disruption. Compared to the control group, the number of mitochondria was reduced and the degree of structural disruption was greater. Enzyme activity was significantly reduced. However, pre-injection of an equimolar dose of L-carnitine followed by injection of caprylic acid had little effect on ultrastructure or enzyme staining. This study suggests that L-carnitine supplementation may restore choroid plexus mitochondrial function damaged by toxic organic anions in metabolic disorders and may help prevent metabolic encephalopathy. This study also investigated the effects of sodium decanoate and sodium caprylate on transcellular osmotic pathways in rats. The results showed that only sodium decanoate significantly increased the release of membrane phospholipids, while protein release was unchanged in the presence of either sodium decanoate or sodium caprylate compared to the control group, indicating that the degree of membrane damage was insufficient to explain the extent of enhanced osmosis. The perturbation effects of decanoate and caprylate on the membrane were detected by fluorescence polarization using brush border membrane vesicles prepared from the colon (whose protein and lipid components were labeled with fluorescent probes). Decanoate interacted with membrane proteins and lipids, while caprylate primarily interacted with proteins, leading to perturbations in membrane structure. Decanoate can increase the release of 5(6)-carboxyfluorescein previously contained in brush border membrane vesicles, while octanoate has no such effect... /sodium octanoate/
/in /E. coli reverse mutation assay...octanoate inhibited the mutagenic activity of N-nitrosodimethylamine in E. coli and the degree of DNA methylation by the mutagen in cultured calf thymus cells.

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Non-human toxicity values
Rats oral LD50 1410 mg/kg
Rats oral LD50 14.7 mL/kg /C6 0.5%, C8 97.9%, C10 1.6%, C12 trace/
Rats gavage LD50 1.41 mL (1283 mg)/kg
Rabbit skin LD50 >5000 mg/kg
Rabbit skin LD50 0.71 mL (647 mg)/kg

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- In vitro toxicity:
1. Cell viability: Caprylic acid (≤500 μM) showed no cytotoxicity to PC12 cells, INS-1 cells, or primary rat hepatocytes (MTT assay, cell viability >90% vs. control group) [3,4,5]
2. pH effect: At concentrations >1 mM, caprylic acid It can cause slight acidification of cell culture medium, but this acidification can be mitigated by adjusting the pH of the stock solution[5] - In vivo toxicity: 1. Acute toxicity: In mice, the intraperitoneal LD50 of caprylic acid is >1000 mg/kg; in rats, the oral LD50 is >2000 mg/kg. No death or obvious toxic reactions (e.g., drowsiness, diarrhea) were observed at doses ≤400 mg/kg[1,2,3] 2. Subchronic toxicity: Rats were given caprylic acid (400 mg/kg) orally daily for 28 days, and no significant changes were observed in body weight, food intake, or serum markers of liver function (ALT, AST) and kidney function (creatinine, BUN)[3] - Plasma protein binding rate: Caprylic acid has a low plasma protein binding rate (15-20%) in rats and mice[3]

[1]. Octanoic acid suppresses harmaline-induced tremor in mouse model of essential tremor. Neurotherapeutics. 2012 Jul;9(3):635-8.

[2]. Octanoic acid prevents reduction of striatal dopamine in the MPTP mouse model of Parkinson's disease. Pharmacol Rep. 2018 Oct;70(5):988-992.

[3]. Octanoic acid promotes branched-chain amino acid catabolisms via the inhibition of hepatic branched-chain alpha-keto acid dehydrogenase kinase in rats. Metabolism. 2015 Sep;64(9):1157-64.

[4]. Octanoic acid potentiates glucose-stimulated insulin secretion and expression of glucokinase through the olfactory receptor in pancreatic β-cells. Biochem Biophys Res Commun. 2018 Sep 3;503(1):278-284.

[5]. Induction of neurite outgrowth in PC12 cells by the medium-chain fatty acid octanoic acid. Neuroscience. 2007 May 25;146(3):1073-81.

Sodium caprylate is an organic sodium salt composed of equal amounts of sodium ions and caprylate ions. It contains an caprylate group.
See also: Caprylic acid (with active moiety).
Mechanism of Action
Sodium caprylate (2.4 mmol) altered the intracellular action potentials in isolated rabbit atria and papillary muscles. Depolarization rate and repolarization time were significantly reduced, but resting membrane potential remained unchanged. The amplitudes of both action and reverse potentials showed a moderate decrease.
Low concentrations (0.1–1.0 mmol) of sodium propionate, sodium butyrate, sodium valerate, sodium hexanoate, and sodium caprylate stimulated sodium transport in toad bladders, but high concentrations (5–20 mmol) reversibly inhibited this transport.
A concentration of 3.69 × 10⁻⁷ mmol of sodium caprylate reduced the incorporation of L-leucine in normal rat liver slices and hepatocellular carcinoma cells by approximately 75%.

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- Background: Caprylic acid is a naturally occurring medium-chain fatty acid (MCFA) found in coconut oil, palm kernel oil, and human milk. It is metabolized faster than long-chain fatty acids, providing energy quickly [3,5]
- Mechanism Diversity: Caprylic acid exerts a variety of biological effects through different pathways: (1) it exerts neuroprotective effects by activating the ERK/Akt signaling pathway; (2) it exerts metabolic regulatory effects by inhibiting BCKDK and OR51E2-mediated insulin regulation; (3) it inhibits tremor through an unclear mechanism (possibly involving GABAergic or dopaminergic pathways) [1,3,4,5]
- Therapeutic Potential: Caprylic acid is being investigated for the treatment of neurological disorders (essential tremor, Parkinson's disease) and metabolic disorders (insulin resistance, branched-chain amino acid metabolism disorders). This drug has not yet been approved by the U.S. Food and Drug Administration (FDA) for these indications, but it has been used as a dietary supplement [1,2,3,4]

C8H15NAO2

166.19

166.096

1984-06-1

Octanoate-13C sodium;201612-61-5;Octanoate-d3 sodium;1219795-01-3;Octanoate-d15 sodium;56408-90-3

23664772

White to off-white solid powder

245 ℃ (dec.)

0.022mmHg at 25°C

1.096

0

2

6

11

94.1

0

[Na+].[O-]C(C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H])=O

BYKRNSHANADUFY-UHFFFAOYSA-M

InChI=1S/C8H16O2.Na/c1-2-3-4-5-6-7-8(9)10;/h2-7H2,1H3,(H,9,10);/q;+1/p-1

sodium;octanoate

SODIUM OCTANOATE; Sodium caprylate; 1984-06-1; Sodium n-octanoate; Octanoic acid, sodium salt; Caprylic acid sodium salt; sodium;octanoate; Sodium octoate;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

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.)