5-HT1A Receptor ( pIC50 = 8.19 ); 5-HT7 Receptor ( pIC50 = 466 nM )
The primary target of 8-OH-DPAT hydrobromide is the 5-HT1A receptor, a G protein-coupled receptor widely distributed in the brain that participates in various physiological functions including mood regulation, body temperature control, blood pressure regulation, and feeding behavior. As a potent agonist of the 5-HT1A receptor, the compound binds to and activates this receptor, leading to downstream effects such as alterations in the cAMP signaling pathway. Additionally, 8-OH-DPAT has moderate affinity for the 5-HT7 receptor (pKi = 6.6), but exhibits very weak activity at the 5-HT1B and 5-HT receptors (pIC50 values of 5.42 and <5, respectively).

At doses less than 100 nM, 8-OH-DPAT hydrobromide (8-Hydroxy-DPAT) has no effect on 5-HT1B binding [1].

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In vitro activity: The medication only shows a slight improvement in the 5-HT1B subtype; 5.42 ± 0.08 (n = 5) is the pIC50. Because 8-OH-DPAT does not affect 5-HT1B binding at concentrations below 100 nM[1]. In cultured human RPE cells, 8-OH-DPAT can lower oxidative damage, boost antioxidant defense, and decrease the accumulation of lipofuscin derived from both autophagic and photoreceptor outer segment sources[4].

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In vitro, 8-OH-DPAT hydrobromide displays potent agonistic activity at the 5-HT1A receptor, with an EC50 of 12 nM in rat hippocampal membranes. At concentrations below 100 nM, it has no effect on 5-HT1B binding. At concentrations of 10 µM and 50 µM, the compound mimics the effects of serotonin, reducing excitatory post-synaptic potentials (EPSPs) in layers II and III of the entorhinal cortex. In cultured human retinal pigment epithelial cells, 8-OH-DPAT reduces oxidative damage, enhances antioxidant defenses, and decreases lipofuscin accumulation.

In animals exposed to 3,4-methylenedimethamphetamine (MDMA), the highest doses of 8-OH-DPAT hydrobromide (8-Hydroxy-DPAT) hydrobromide (32, 56, 80, and 100 mg/kg; surgical injection; 15 minutes before testing) significantly interfered with sustained focus and Reinforcing effect (gradual entry range; PR), but not in control animals [1].

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The selective 5-HT1A-receptor agonist 8-OH DPAT, when injected intravenously, quickly and with little variability reverses the bradycardic and hypotensive responses that are established during severe bleeding. The blood-brain barrier can be easily crossed by 8-OH-DPAT because it is comparatively lipophilic[3].

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Central administration of serotonergic 5-HT1A receptor agonists delays the reflex sympatholytic response to severe hemorrhage in conscious rats. To determine the region where 5-HT1A receptor agonists act to mediate this response, recovery of mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) was compared in hemorrhaged rats after injection of the selective 5-HT1A agonist, (+)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH DPAT), in various regions of the cerebroventricular system or the systemic circulation. Three minutes after injection of 8-OH-DPAT (48 nmol/kg), MAP and RSNA were higher in hemorrhaged rats given drug in the fourth ventricle (94 +/- 5 mmHg, 82 +/- 18% of baseline) or the systemic circulation (90 +/- 4 mmHg, 113 +/- 15% of baseline) than in rats given drug in the Aqueduct of Sylvius (63 +/- 4 mmHg, 27 +/- 11% of baseline), the lateral ventricle (42 +/- 3 mmHg, -8 +/- 18% of baseline), or in rats given saline in various brain regions (47 +/- 5 mmHg, -42 +/- 10% of baseline). A lower-dose injection of 8-OH DPAT (10 nmol/kg) also accelerated the recovery of MAP and RSNA in hemorrhaged rats when given in the fourth ventricle (94 +/- 26 mmHg, 72 +/- 33% of baseline 3 min after injection) but not the systemic circulation (46 +/- 4 mmHg, -25 +/- 30% of baseline). These data indicate that 8-OH DPAT acts on receptors in the hindbrain to reverse the sympatholytic response to hemorrhage in conscious rats. [3]

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5-HT1A agonist 8-OH DPAT mediates neuroprotection in a mouse model of AMD. 5-HT1A agonist 8-OH DPAT reduces lipofuscin accumulation in vivo. [4]

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In in vivo animal models, 8-OH-DPAT exhibits a variety of pharmacological activities. In mouse studies, direct administration into the dorsal raphe nucleus reduces attack bites in a baclofen-induced model of aggressiveness; administration at 0.5 mg/kg impairs contextual fear conditioning; and at 50 µg/kg, it reduces the incidence of apnea and improves respiratory regularity in a methyl-CpG-binding protein 2-deficient mouse model of Rett syndrome. In a rat model of diabetes, the compound enhances bradycardia in response to vagal electrical stimulation. Additionally, rapid intravenous injection of 8-OH-DPAT quickly reverses vagal bradycardia and hypotensive responses during severe hemorrhage. R(+)-8-OH-DPAT hydrobromide (0.05 mg/kg, s.c.) potentiates SUL-induced dopamine (DA) release in the medial prefrontal cortex (mPFC).

8-OH-DPAT (also known as 8-Hydroxy-DPAT) is a well-established, strong, and specific 5-HT1A agonist, with a pIC50 of 8.19. 8-OH-DPAT weakly binds to 5-HT1B with pIC50 of 5.42 and pIC50 <5 for 5-HT; it has a selectivity of almost a thousand times for a subtype of the 5-HT1 binding site and a Ki of 466 nM for 5-HT7. Furthermore In cultured human RPE cells, it can decrease oxidative damage, boost antioxidant defense, and lessen the accumulation of lipofuscin produced by both autophagy and photoreceptor outer segment. In orexin-KO mice, narcoleptic-like sleep dysfunction is caused by 5-HT1A receptor dysfunction, which may also contribute to orexin deficiency-induced sleep disorders. In addition, the use of 5-HT1A receptor agonists like 8-OH-DPAT may be helpful in treating sleep disorders caused by orexin deficiencies.

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Receptor binding assays typically employ radioligand binding methods. For example, using membrane preparations from HEK293 cells expressing recombinant human 5-HT1A receptors (50-70 µg protein), the membranes are resuspended in binding buffer containing 20 mM HEPES, 3 mM MgSO4, and 120 mM NaCl (pH 7.4). The membranes are incubated with 30 µM GDP and various concentrations (0.1 nM to 10 µM) of test compounds or 8-OH-DPAT (reference curve) for 20 min at 30°C in a final volume of 0.5 mL. Then, [³⁵S]GTPγS (200 pM) is added, and the samples are incubated for an additional 30 min at 30°C. Nonspecific binding is determined in the presence of 10 mM GTPγS. The reaction is terminated by the addition of ice-cold HEPES buffer, followed by rapid vacuum filtration onto Unifilter B filters. The filters are washed with ice-cold HEPES buffer, and retained radioactivity is measured by liquid scintillation counting. Alternatively, [³H]8-OH-DPAT can be used as the radioligand, incubated with membrane preparations in 20 mM HEPES buffer (pH 7.0, containing 5 mM MgCl₂) for 150 min at room temperature, followed by vacuum filtration through 0.3% polyethyleneimine-pretreated filters and scintillation counting to determine binding parameters (Kd and Bmax).

Cells are exposed to H2O2 (200 µM) for 1 hour and either pre-or post treated with 8-OH DPAT (10 µM) for 24 hours. All measurements for the pretreatment phase are taken 24 hours after the H2O2 exposure, and for the posttreatment phase, 8-OH DPAT is added right away. Management of 5HT1A agonists: Addition of 8-OH DPAT, a 5-HT1A receptor agonist, to the culture medium at concentrations ranging from 0.1 to 20 µM is done every 48 hours to evaluate the compound's capacity to inhibit lipofuscin formation in cultured stem cells. PBS-only-receiving cells served as negative controls in all experiments, which were conducted in basal medium. In order to find out if the effects of 8-OH DPAT persist after 5-HT1A receptor agonist treatment is stopped, the cells are kept in basal medium or fed POS for an additional 28 days after the 8-OH DPAT treatment is stopped. In order to determine whether 8-OH DPAT can eliminate lipofuscin that has already been present, autophagy- and phagocytic-derived lipofuscin are allowed to build up as previously mentioned, and then 8-OH DPAT is added every two days for a maximum of 28 days. We include the 5-HT1A receptor antagonist S(-)-UH-301 at 5 µM in some experiments to verify that 8-OH DPAT is acting through the 5-HT1A receptor agonist. In order to ascertain how the timing of 8-OH DPAT treatment affects oxidative stress markers, RPE cultures are either treated with the 5HT1A agonist for 3 or 24 hours following exposure to H2O2 or pre-treated with 8-OH DPAT (at 1 or 10 µM) for 3 or 24 hours prior to exposure to 200 µM H2O2 for 1 hour. As a negative control, cells that are not subjected to an oxidative stressor are used, and as a positive control, cells that are subjected to an oxidative stressor but do not receive 8-OH DPAT. The only function of cells exposed to 8-OH DPAT is that of an extra control.

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For in vitro cell assays, recombinant cell lines expressing the 5-HT1A receptor (e.g., HEK293 cells) are typically used for functional assays. Cells are cultured in DMEM medium containing 10% fetal bovine serum and antibiotics at 37°C with 5% CO₂ in a humidified incubator. Prior to the experiment, cells are seeded into 96-well plates and cultured overnight. Different concentrations of 8-OH-DPAT hydrobromide (generally from 10⁻¹⁰ M to 10⁻⁵ M, prepared in DMSO with final DMSO concentration ≤0.1%) are added, and the cells are further incubated for 30 min to 2 hours. Downstream signaling is then measured, such as determination of intracellular cAMP levels using a cAMP detection kit (since 5-HT1A is a Gi-coupled receptor, agonists inhibit forskolin-stimulated cAMP accumulation), or measurement of intracellular calcium flux using calcium-sensitive fluorescent probes. After the reaction, fluorescence or chemiluminescence signals are read using a multi-mode microplate reader, and EC50 values and maximal effects are calculated.

Mice: An infrared sensor installed in each mouse's home cage monitors the animals' locomotor activity. Locomotor activity is recorded at 30-min intervals beginning at 8:00 a.m. and 8:00 p.m., respectively, to compare the activity during the light and dark periods. All medications are given at 8:00 p.m., and locomotor activity is then monitored for three hours to determine the effects of psychostimulants (8-OH-DPAT, 1, 3 mg/kg, s.c., etc.) on this activity during the dark period.

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Experimental Design [2]
Before the experiment, the animals were connected to the recording instrumentation and a withdrawal pump while resting unrestrained in their home cage. The injector containing drug for brain injection was filled with appropriate fluid and placed in the guide cannula before habituation. The rat was then allowed to rest undisturbed for at least 2 h before hemorrhage. Arterial pressure, HR, and RSNA were recorded continuously beginning 10 min before the hemorrhage and ending 20 min after hemorrhage termination. Controlled blood withdrawal was initiated at a rate of 3.2 ml · min−1 · kg−1for 6 min, after which the speed was reduced to 0.53 ml/min for an additional 4 min. In preliminary tests, this procedure was found to produce a consistent fall in MAP, HR, and RSNA after withdrawal of ∼11.2 ml/kg blood or ∼14% of estimated blood volume. The subsequent change to the lower rate of withdrawal was sufficient to maintain bradycardic and sympatholytic responses until hemorrhage termination.[2]
After the initiation of blood withdrawal (7 min), 48 nmol/kg 8-OH DPAT (in 0.5 μl saline) or an equivalent volume of saline was injected over 20 s in either the lateral ventricle, the Aqueduct of Sylvius, or the fourth ventricle. In a fourth group, drug or vehicle was injected intravenously in a volume of 5 μl and flushed with an additional 100 μl of saline over 20 s. All injections were made remotely via tubing that extended outside the cage. After drug injection, no further intervention or resuscitation was performed before termination of the experiment. The dose of 8-OH DPAT chosen for use in these initial studies corresponded to the ED50determined in prior experiments to increase the volume of blood withdrawal that produced a 40-mmHg fall in blood pressure when injected in the lateral ventricle 15 min before hemorrhage. In a separate set of experiments, responses to a lower dose (10 nmol/kg) injection of 8-OH DPAT in the fourth ventricle or systemic was assessed after hemorrhage in the same manner. An additional sham-hemorrhage group, instrumented in the same manner, was injected with 10 nmol/kg 8-OH-DPAT in the fourth ventricle without prior hemorrhage.[2]
After termination of the experiment, rats were killed with an overdose of pentobarbital sodium (100 mg/kg iv). Cannulated rats were subsequently given intercerebroventricular injections of 0.5 μl toliudine blue (0.5%). The brains were removed quickly and postfixed in 10% formalin overnight. The brains were cut the following day to confirm proper cannula placement. Only data from animals in which dye was found to have diffused through the ventricular system (i.e., dye was not injected in tissue) were included in the data analysis.

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Effect of 8-OH DPAT in the SOD2 knockdown model for AMD [4]
Mice were randomly assigned to one of three groups and received daily subcutaneous injections of either sterile saline, 0.5 mg/kg body weight 8-OH DPAT in sterile saline (low dose), or 5.0 mg/kg 8-OH DPAT (high dose). At monthly intervals mice were evaluated by digital fundus imaging, full-field scotopic (dark adapted) electroretinography (ERG) and spectral domain optical coherence tomography (SD-OCT). At four months, mice were euthanized and eyes were prepared for cryosectioning. Confocal microscroscopy was used to measure autofluorescence in the RPE layer of untreated eyes and virus-treated eyes with or without 8-OH DPAT. Excitation frequency was 387 nm and emission frequency was 440–684 nm and fluorescence intensity was assessed using ImageJ. Sections were also used to assess damage to retinal structure by light microscopy and immunostaining for 8-Oxo-2′-deoxyguanosine (8OHdG) (Abcam, Cambridge, MA, USA) as a measurement of oxidative stress using previously described methodology

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An example in vivo experimental protocol using male Sprague-Dawley rats (250-350 g): 8-OH-DPAT hydrobromide is dissolved in sterile saline (with a small amount of DMSO for solubilization if needed, e.g., DMSO:Tween 80:Saline = 10:5:85) and administered at 0.05 mg/kg (subcutaneous injection). Animals are allowed to acclimate to the experimental environment for 30 minutes prior to the experiment and observed after drug administration. Behavioral parameters (e.g., body temperature changes, 5-HT syndrome behavior scores) are recorded at various time points (e.g., 0, 15, 30, 60, 120 minutes) after administration. For detection of neurotransmitter release in the brain, microdialysis technique can be used to collect dialysate from the medial prefrontal cortex (mPFC), followed by HPLC with electrochemical detection to measure dopamine (DA) and its metabolite levels. An alternative model: 8-OH-DPAT is dissolved in 10 mL of saline and administered at 0.8 mg/(kg·day) via intrathecal injection into the lumbosacral spinal subarachnoid space for 4 weeks to establish a rat model of premature ejaculation.

The pharmacokinetic profile of 8-OH-DPAT hydrobromide is characterized by a biological half-life of approximately 1.5 hours, with rapid absorption, distribution, metabolism, and excretion (ADME) processes. The compound is lipophilic and can readily cross the blood-brain barrier. A pharmacokinetic study in goats showed that following intramuscular administration of 0.1 mg/kg R-8-OH-DPAT hydrobromide, the mean bioavailability was 66%, the mean volume of distribution in the central compartment was 1.47 L/kg, and the mean plasma body clearance was 0.056 L/kg/min. All goats administered intravenously exhibited signs of serotonin toxicity, suggesting that dosages should be appropriately reduced for clinical use. The metabolic pathways mainly involve oxidative metabolism and conjugation reactions.

According to the Material Safety Data Sheet (MSDS), 8-OH-DPAT hydrobromide is classified as toxic, containing a pharmaceutically active ingredient. Safety hazards include: risk of serious damage to eyes (R41) and danger of serious damage to health by prolonged exposure (R48). In case of skin contact, flush with copious amounts of water; in case of eye contact, remove contact lenses and flush with copious amounts of water. If inhaled, move the patient to fresh air and administer artificial respiration if breathing stops. Thermal decomposition may produce toxic fumes such as carbon monoxide, carbon dioxide, and nitrogen oxides. In animal studies, administration of R-8-OH-DPAT hydrobromide at a dosage of 0.1 mg/kg resulted in clinical signs of serotonin toxicity in goats, indicating that the compound carries potential risks of neurological toxicity. Handling should be performed using chemical-resistant gloves, safety goggles, and in a well-ventilated area.

[1]. 8-Hydroxy-2-(di-n-propylamino)-tetralin discriminates between subtypes of the 5-HT1 recognition site. Eur J Pharmacol. 1983 May 20;90(1):151-3.

[2]. 5-HT1A agonists and dopamine: the effects of 8-OH-DPAT and buspirone on brain-stimulation reward. J Neural Transm Gen Sect. 1991;83(1-2):139-48.

[3]. 5-HT1A receptor agonist 8-OH-DPAT acts in the hindbrain to reverse the sympatholytic response to severe hemorrhage. Am J Physiol Regul Integr Comp Physiol. 2003 Mar;284(3):R782-91.

[4]. The 5HT1a receptor agonist 8-Oh DPAT induces protection from lipofuscin accumulation and oxidative stress in the retinal pigment epithelium. PLoS One. 2012;7(4):e34468.

[5]. Cognitive performance of MDMA-treated rhesus monkeys: sensitivity to serotonergic challenge. Neuropsychopharmacology. 2002 Dec;27(6):993-1005.

8-OH-DPAT is a serotonin 1A receptor agonist commonly used in experiments to test the effects of serotonin. 8-OH-DPAT is a tetrahydronaphthalene with hydroxyl and dipropylamino groups substituted at positions 1 and 7, respectively. It is a serotonergic antagonist. It belongs to the tetrahydronaphthalene class of compounds, phenolic compounds, and tertiary amine compounds. It is derived from the hydride of tetrahydronaphthalene. This study tested the effects of two specific 5-HT1A receptor agonists, 8-OH-DPAT (0-300 μg/kg) and buspirone (0-3.0 mg/kg), on the self-stimulation of variable time-threshold currents in the lateral hypothalamus of rats. Buspirone resulted in sustained monotonic inhibition of the response, while the effect of 8-OH-DPAT was biphasic: a dose of 3.0 μg/kg led to sustained enhancement of the response, while higher doses (100–300 μg/kg) resulted in relatively transient inhibition. This biphasic pattern is consistent with previously reported effects of 8-OH-DPAT on food intake and various other behaviors. Threshold current self-stimulation was highly sensitive to alterations in dopaminergic transmission but relatively insensitive to changes in serotonin (5-HT). Therefore, the most plausible explanation for the stimulating effect of low-dose 8-OH-DPAT appears to be enhanced dopaminergic transmission. This may be due to inhibition of 5-HT release mediated by the 5-HT1A autoreceptor and the resulting de-inhibition of dopaminergic transmission. The inhibitory effect of high-dose 8-OH-DPAT on self-stimulation may reflect the activity of 8-OH-DPAT on postsynaptic 5-HT receptors, thereby inhibiting dopamine (DA) transmission. The inhibitory effect of buspirone on the response at all tested doses may reflect the compound’s role as a partial agonist of postsynaptic 5-HT receptors and/or its effects on other systems. [2] Age-related macular degeneration (AMD) is one of the leading causes of blindness in older adults and is associated with oxidative stress, lipofuscin accumulation, and retinal degeneration. This study aimed to determine whether 5-HT(1A) receptor agonists could reduce lipofuscin accumulation, mitigate oxidative damage, and prevent retinal cell loss in vitro and in vivo. Flow cytometry (FACS) and confocal microscopy were used to evaluate the formation of autophagy-derived and photoreceptor outer segment (POS)-derived lipofuscin in cultured retinal pigment epithelium (RPE) cells with or without the 5-HT(1A) receptor agonist 8-OH DPAT. Compared with the control group, 8-OH DPAT treatment resulted in a dose-dependent reduction in both autophagy-derived and POS-derived lipofuscin. The reduction in autophagy-induced lipofuscin could be sustained for up to 4 weeks after drug withdrawal. Furthermore, the ability of 8-OH DPAT to mitigate oxidative damage after treatment with 200 µM H₂O₂ was evaluated. Compared with the control group, 8-OH DPAT reduced superoxide production in H₂O₂-treated cells, increased mitochondrial superoxide dismutase (MnSOD) levels and the ratio of reduced to oxidized glutathione, and protected cells from H₂O₂-induced lipid peroxidation, elevated nitrotyrosine levels, and mitochondrial damage. SOD2 knockout mice with an AMD-like phenotype were subcutaneously injected daily with saline, 0.5 or 5.0 mg/kg of 8-OH DPAT, and evaluated monthly. Compared with injectable vector-mediated SOD2 knockout mice, systemic injection of 8-OH DPAT improved electroretinogram responses in the eyes of SOD2 knockout mice. Compared with the untreated control group, mice treated with 8-OH DPAT showed a significant increase in ONL thickness and a 60% reduction in RPE lipofuscin 4 months after MnSOD knockdown. These data suggest that 5-HT(1A) receptor agonists can reduce lipofuscin accumulation and protect the retina from oxidative damage and mitochondrial dysfunction. 5-HT(1A) receptor agonists may have the potential to be used as drugs for the treatment of retinal degenerative diseases. [4]

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C16H26BRNO

328.2877

327.12

C, 58.54; H, 7.98; Br, 24.34; N, 4.27; O, 4.87

76135-31-4

8-OH-DPAT;78950-78-4; 76135-31-4 (HBr); 141215-27-2 (HCl)

6917794

White to off-white solid powder

4.329

2

2

5

19

237

0

BATPBOZTBNNDLN-UHFFFAOYSA-N

InChI=1S/C16H25NO.BrH/c1-3-10-17(11-4-2)14-9-8-13-6-5-7-16(18)15(13)12-14;/h5-7,14,18H,3-4,8-12H2,1-2H3;1H

7-(dipropylamino)-5,6,7,8-tetrahydronaphthalen-1-ol;hydrobromide

76135-31-4; 8-Hydroxy-DPAT hydrobromide; 8-OH-DPAT HRr; 8-Hydroxy-2-dipropylaminotetralin hydrobromide; 8-OH-dpat hydrobromide; 87394-87-4; UNII-G8TFV2F5CP; G8TFV2F5CP;

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)

DMSO : ~25 mg/mL (~76.15 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.)