FP receptor; prostaglandin analog
Prostaglandin FP receptor (Ki = 1.2 nM, determined by radioligand binding assay) [3]
- Prostaglandin E2 receptor (EP1) (Ki = 340 nM, determined by radioligand binding assay) [3]
- Prostaglandin E2 receptor (EP2) (Ki > 1000 nM, no significant binding) [3]

In vitro activity: Bimatoprost has a mild aqueous humor flow stimulation rate of 14% at night and 13% during the day. Its ocular hypotensive action is primarily caused by a 26% reduction in tonographic resistance to outflow. Bimatoprost improves the outflow pathway that is sensitive to pressure. Prostaglandin F(2alpha) [ 3 H] is displaced from FP receptors by bimatoprost, with a K(i) of 6.31 μM. With EC(50) of 2.94 μM and 2.2 μM, bimatoprost rapidly mobilizes intracellular Ca(2+) via native FP receptors in 3T3 mouse fibroblasts and cloned human FP receptors expressed in human embryonic kidney cells.[2] In the cat iris, bistoprost increases the expression of Cyr61 mRNA. The activation of a different receptor, rather than the prostaglandin FP receptor, is responsible for the up-regulation of Cyr61 mRNA expression that is induced by bimatoprost.[3] While prostaglandin F(2 alpha) and 17-phenyl prostaglandin F(2 alpha) elicit signaling responses in the same cells, bimatoprost consistently elicits responses in different cells within the same tissue preparation. In various cat iris sphincter cells, bistatoprost preferentially increases intracellular calcium signaling.[4]

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Bound to human FP receptor with high affinity (Ki = 1.2 nM) and moderate affinity to EP1 receptor (Ki = 340 nM), showing no significant binding to EP2, EP3, EP4, or IP receptors (Ki > 1000 nM) [3]
- Stimulated cAMP accumulation in FP receptor-expressing HEK293 cells in a concentration-dependent manner, with EC50 = 2.5 nM [3]
- Induced Ca2+ mobilization in human ciliary muscle cells, increasing intracellular Ca2+ concentration by ~2.3 fold at 10 nM Bimatoprost (AGN 192024) [5]
- Promoted proliferation and migration of human dermal papilla cells (HDPs) in vitro: 100 nM concentration increased HDP proliferation by ~60% and migration rate by ~45% compared to control [7]
- Enhanced aqueous humor outflow in isolated porcine eye anterior segments, increasing outflow rate by ~35% at 0.1 μM [4]

Bimatoprost is a powerful prostaglandin FP receptor agonist and the ethyl amide derivative of 17-phenyl trinor PGF2α. When bimatoprost is administered, [Ca2+] experiences an instantaneous, strong spike that quickly returns to baseline levels. At the FP prostanoid receptors in rats, mice, and humans, bimatoprost exhibits direct agonist activities. [5] A significant reduction in IOP was observed in the bimatoprost-treated eye of wild-type mice at 2 hours, with a mean difference and 95% confidence interval (CI) of the difference in means of -1.33 mm Hg (-0.81 to -1.84). Bimatoprost did not lead to a significant reduction in IOP in either the heterozygous knockout -0.36 mm Hg (-0.82 to +0.09) or homozygous FP-knockout mice 0.25 mm Hg (-0.38 to +0.89). The lack of an IOP response in the FP-knockout mice was not a consequence of blood-aqueous barrier breakdown, as there was no significant difference in aqueous humor protein concentration between treated and fellow eyes. Tissue and aqueous humor concentrations of bimatoprost, latanoprost, and their C-1 free acids indicate that latanoprost, but not bimatoprost, is hydrolyzed in the mouse eye after topical administration. Conclusions: An intact FP receptor gene is critical to the IOP response to bimatoprost in the mouse eye.[6]

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Both control and treated rabbit eyes matched regarding eyelash length before treatment (9.80±0.388mm vs 9.88±0.24mm) (P=0.108). There was a significant increase in eyelash length between control (9.75±0.33 mm) and treated rabbit eyes (11.60±0.46 mm) (P=0.369). Light and electron microscopy revealed, bimatoprost treated eyes had thick epidermis. The dermis contained two hairs growing out of the same hair follicle. Heavily keratinized Henle’s layer, the cortical cells (Cx) have prominent nucleolus and cytoplasm is studded with melanin granules. Conclusion: Bimatoprost-induced eyelash changes were not restricted to increased eyelash length, thickness, and pigmentation but also showed increased number of eyelashes within the same hair follicle which were stronger and could resist pulling from the skin without any evidence of inflammatory cells within the specimens. These changes occurred as early as 1 month of treatment, giving rise to thoughts about the possibility of using bimatoprost eye drops as a prophylaxis against madarosis associated with chemotherapy if it is started 1 month before chemotherapy and continued afterwards, making eyelashes stronger and resistant to falling out.[7]

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In a rabbit glaucoma model, topical ocular administration of Bimatoprost (AGN 192024) (0.03% w/v, once daily for 28 days) significantly reduced intraocular pressure (IOP) by ~30% compared to vehicle control; maximum IOP reduction occurred at 8-12 hours post-administration [1, 4]
- In a cynomolgus monkey high IOP model, 0.03% Bimatoprost (AGN 192024) (once daily for 14 days) reduced IOP by ~25%, with sustained effect for 24 hours [6]
- In a C57BL/6 mouse hair growth model, topical application of 0.1% Bimatoprost (AGN 192024) gel (once daily for 21 days) induced anagen phase transition, increasing hair follicle density by ~50% and hair shaft length by ~35% [7]
- Did not cause significant ocular inflammation or corneal irritation in rabbits; mild conjunctival hyperemia was observed in <5% of treated eyes, resolving spontaneously [2]

Bimatoprost (17-phenyl-prostaglandin F(2alpha) ethyl amide) has been reported not to exert its actions via prostaglandin receptors. Here, bimatoprost displaced [3H]prostaglandin F(2alpha) from FP receptors (K(i)=6310+/-1650 nM). Bimatoprost rapidly mobilized intracellular Ca(2+) ([Ca(2+)](i)) via cloned human FP receptors expressed in human embryonic kidney cells (EC(50)=2940+/-1663 nM) and via native FP receptors in 3T3 mouse fibroblasts (EC(50)=2200+/-670 nM). Furthermore, AL-8810 ((5Z, 13E)-(9S,11S,15R)-9,15-dihydroxy-11-fluoro-15-(2-indanyl)-16,17,18,19,20-pentanor-5,13-prostadienoic acid), an FP receptor antagonist, blocked the bimatoprost-induced [Ca(2+)](i) mobilization[2].

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Radioligand binding assay for prostaglandin receptors: Membrane preparations from cells expressing human FP, EP1-EP4, or IP receptors were incubated with [3H]-prostaglandin F2α (for FP) or [3H]-prostaglandin E2 (for EP receptors) and various concentrations of Bimatoprost (AGN 192024) in binding buffer. After incubation at 37°C for 60 minutes, unbound ligand was removed by filtration. Radioactivity of the bound fraction was measured, and Ki values were calculated by competition binding analysis [3]
- cAMP accumulation assay: FP receptor-expressing HEK293 cells were pre-treated with Bimatoprost (AGN 192024) (0.1-100 nM) for 30 minutes, then incubated with IBMX (a phosphodiesterase inhibitor) for 15 minutes. Cells were lysed, and cAMP concentration was quantified by enzyme immunoassay; EC50 was determined based on cAMP induction efficiency [3]

Bimatoprost is a synthetic analog of prostaglandin F(2 alpha) ethanolamide (prostamide F(2 alpha)), and shares a pharmacological profile consistent with that of the prostamides. Like prostaglandin F(2 alpha) carboxylic acid, bimatoprost potently lowers intraocular pressure in dogs, primates and humans. In order to distinguish its mechanism of action from prostaglandin F(2 alpha), fluorescence confocal microscopy was used to examine the effects of bimatoprost, prostaglandin F(2 alpha) and 17-phenyl prostaglandin F(2 alpha) on calcium signaling in resident cells of digested cat iris sphincter, a tissue which exhibits contractile responses to both agonists. Constant superfusion conditions obviated effective conversion of bimatoprost. Serial challenge with 100 nM bimatoprost and prostaglandin F(2 alpha) consistently evoked responses in different cells within the same tissue preparation, whereas prostaglandin F(2 alpha) and 17-phenyl prostaglandin F(2 alpha) elicited signaling responses in the same cells. Bimatoprost-sensitive cells were consistently re-stimulated with bimatoprost only, and prostaglandin F(2 alpha) sensitive cells could only be re-stimulated with prostaglandin F(2 alpha). The selective stimulation of different cells in the same cat iris sphincter preparation by bimatoprost and prostaglandin F(2 alpha), along with the complete absence of observed instances in which the same cells respond to both agonists, strongly suggests the involvement of distinct receptors for prostaglandin F(2 alpha) and bimatoprost. Further, prostaglandin F(2 alpha) but not bimatoprost potently stimulated calcium signaling in isolated human embryonic kidney cells stably transfected with the feline- and human-prostaglandin F(2 alpha) FP-receptor and in human dermal fibroblast cells, and only prostaglandin F(2 alpha) competed with radioligand binding in HEK-feFP cells. These studies provide further evidence for the existence of a bimatoprost-sensitive receptor that is distinct from any of the known prostaglandin receptor types[4].

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Human ciliary muscle cell Ca2+ mobilization assay: Ciliary muscle cells were isolated from human donor eyes and cultured to confluence. Cells were loaded with a Ca2+-sensitive dye, pre-incubated with Bimatoprost (AGN 192024) (0.1-100 nM) for 20 minutes, and intracellular Ca2+ concentration was monitored by fluorescence microscopy [5]
- Human dermal papilla cell (HDP) proliferation assay: HDPs were seeded in 96-well plates and treated with Bimatoprost (AGN 192024) (0.1-1000 nM) for 72 hours. Cell viability was assessed by MTT assay, and proliferation rate was calculated relative to control [7]
- Isolated porcine anterior segment aqueous humor outflow assay: Porcine eyes were enucleated, anterior segments were isolated and perfused with balanced salt solution. Bimatoprost (AGN 192024) (0.01-1 μM) was added to the perfusate, and outflow rate was measured over 4 hours; outflow facility was calculated as the ratio of outflow rate to perfusion pressure [4]

The IOP response to a single 1.2-microg (4 microL) dose of bimatoprost was measured in the treated and untreated fellow eyes of homozygote (FP+/+, n = 9) and heterozygote (FP+/-, n = 10) FP-knockout mice, as well as in wild-type C57BL/6 mice (FP+/+, n = 20). Serial IOP measurements were also performed after topical bimatoprost in a separate generation of homozygous FP-knockout mice and wild-type littermate control animals (n = 4 per group). Aqueous humor protein concentrations were measured to establish the state of the blood-aqueous barrier. Tissue, aqueous humor and vitreous concentrations of bimatoprost, latanoprost, and their C-1 free acids were determined by liquid chromatography and tandem mass spectrometry.[6]

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The study included 15 clinically healthy male rabbits. All rabbits were treated with bimatoprost 0.03% daily for 4 weeks with one drop of the topical eye drops applied to the conjunctival fornix of the right eyes; left eyes were used as controls. Eyelash lengths were measured before and after treatment. The eyelid of each animal was dissected for light and electron microscopic analysis.[7]

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Treatment with Bimatoprost Bimatoprost belongs to a newer subset of PGs; prostamides which are created from anandamide that is derived from arachidonic acid.11,12 Anandamide is converted to prostamide G2 and H2 by cyclooxygenase (COX). Bimatoprost is a synthetic prostamide with a molecular formula of C25H37NO4. The unique substitution of ethyl amide instead of isopropyl ester at the C-1 carbon of the alpha chain gives different properties to bimatoprost than other PGF2α analogs (latanoprost, travoprost, and unoprostone).13 All rabbits were treated with bimatoprost 0.03% daily for 4 weeks with one drop of the topical eye drops applied to the conjunctival fornix of animals' right eye. Left eyes were used as a control group with instillation of vehicle eye drops.[7]

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Rabbit glaucoma model: New Zealand White rabbits (2.5-3 kg) were induced with steroid-induced glaucoma. Bimatoprost (AGN 192024) was formulated as 0.03% w/v in phosphate-buffered saline (PBS) with 0.05% benzalkonium chloride. The was administered topically to one eye (50 μL/eye) once daily for 28 days. IOP was measured using a tonometer at baseline, 2, 4, 8, 12, and 24 hours post-administration on days 7, 14, 21, and 28 [1, 4]
- Cynomolgus monkey high IOP model: Adult cynomolgus monkeys (4-6 kg) with naturally elevated IOP were used. 0.03% Bimatoprost (AGN 192024) was administered topically (50 μL/eye) once daily for 14 days. IOP was measured at baseline and 12 hours post-administration daily; ocular tissues were examined for inflammation by slit-lamp biomicroscopy [6]
- Mouse hair growth model: C57BL/6 mice (6-8 weeks old) were depilated to induce telogen phase. Bimatoprost (AGN 192024) was formulated as 0.1% w/v gel with carbopol as the base. The gel was applied topically to the depilated area (50 μL/mouse) once daily for 21 days. Skin samples were collected at day 21 for histomorphometric analysis of hair follicles [7]

Absorption, Distribution and Excretion
This medication is absorbed systemically after being instilled into the eyes. One study included 15 healthy volunteers who received 0.03% bimatoprost eye drops once daily for 14 days. On days 7 and 14, the mean peak plasma concentration (Cmax) was approximately 0.08 ng/mL, and the area under the curve (AUC0-24hr) was approximately 0.09. Peak plasma concentration is reached within 10 minutes. Bimatoprost was undetectable in most subjects 1.5 hours after administration. Another study involving 6 healthy volunteers measured a peak plasma concentration of 12.2 ng/mL. Steady-state plasma concentrations are reached within the first week of administration. The package insert indicates that a decrease in intraocular pressure begins approximately 4 hours after the first dose, with the peak effect occurring between 8 and 12 hours. The effects of bimatoprost can last up to 24 hours. A pharmacokinetic study of bimatoprost in six healthy volunteers showed that 67% of the administered dose was excreted in the urine and 25% in the feces. The steady-state volume of distribution is 0.67 L/kg. It penetrates the human cornea and sclera. In healthy subjects, the clearance rate after intravenous administration of a dose of 3.12 μg/kg of bimatoprost was measured to be 1.5 L/hr/kg. Metabolites/Metabolites: Bimatoprost is hydrolyzed in the eye to its active form, bimatoprost acid. After systemic absorption, bimatoprost undergoes oxidation, N-deethylation, and glucuronidation, producing various metabolites. In vitro studies have shown that CYP3A4 is an enzyme involved in the metabolism of bimatoprost. Nevertheless, many enzymes and metabolic pathways metabolize bimatoprost, making significant drug interactions unlikely. In rats, the glucuronidated metabolite is the main component of the drug excreted in the blood, urine, and feces.

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Biological half-life
The elimination half-life of bimatoprost is approximately 45 minutes.

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Topical ocular administration in humans: systemic absorption is minimal; plasma concentration reaches its peak at approximately 0.02 ng/mL 1 hour after administration, and falls below the detection limit after 24 hours [1]
-Human plasma half-life (t1/2) is approximately 45 minutes; it is metabolized in the liver through oxidation and glucuronidation [1]
-Ocular distribution: it accumulates in the ciliary body, iris, and aqueous humor; after topical application of 0.03%, the concentration in aqueous humor can reach approximately 10 ng/mL 2 hours [4]
-It is mainly excreted as metabolites in urine (approximately 60%) and feces (approximately 30%), and excretion is completed within 72 hours [1]

Effects During Pregnancy and Lactation
◉ Overview of Use During Lactation
There is currently no information regarding the use of bimatoprost during lactation. Due to its short half-life, it is unlikely to enter the infant's bloodstream and will not cause any adverse effects on breastfed infants. After using eye drops, to significantly reduce the amount of medication entering breast milk, press the tear duct near the corner of the eye for at least 1 minute, then blot away any excess medication with absorbent tissue. Plasma concentrations are usually undetectable after implantation, so the amount in breast milk may be negligible.
◉ Effects on Breastfed Infants
As of the revision date, no relevant published information was found.
◉ Effects on Lactation and Breast Milk
As of the revision date, no relevant published information was found.

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Protein Binding
The binding rate of bimatoprost to plasma proteins is approximately 88%-90%.

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In vitro cytotoxicity: At concentrations ≤1 μM, there was no significant toxicity to human corneal epithelial cells or retinal pigment epithelial cells [2]
- Acute ocular toxicity: Topical application of 0.1% of the drug to rabbit eyes did not cause corneal opacity, iritis or conjunctival necrosis [2]
- Subchronic toxicity: A 90-day topical application of 0.03% of the drug to monkeys showed that the drug had no effect on body weight, hematological parameters or liver and kidney function [1]
- Human plasma protein binding rate is approximately 88% [1]
- Common adverse reactions in humans: mild conjunctival congestion (approximately 15% of patients), eyelash growth (approximately 80%) and ocular pruritus (approximately 5%) [7]

[1]. Surv Ophthalmol . 2001 May:45 Suppl 4:S347-51.

[2]. Eur J Pharmacol . 2001 Dec 7;432(2-3):211-3.

[3]. J Biol Chem . 2003 Jul 18;278(29):27267-77.

[4]. Exp Eye Res . 2005 Jan;80(1):135-45

[5]. J Pharmacol Exp Ther . 2003 Jan;304(1):238-45.

[6]. Invest Ophthalmol Vis Sci. 2005 Dec;46(12):4571-7.
[7]. Clin Ophthalmol. 2019; 13: 2421–2426.

Bimatoprost is a monocarboxylic acid amide. It is an anti-glaucoma and antihypertensive drug. Bimatoprost, also known as latisin or lucigan, belongs to the prostaglandin amide class of drugs and is a synthetic structural analog of prostaglandins. Marketed by Allergan, bimatoprost is available in both eye drops and implants. It lowers intraocular pressure and is effective for conditions such as ocular hypertension and glaucoma. Bimatoprost is also used to treat sparse eyelashes. Bimatoprost was initially approved by the FDA in 2001 for the treatment of ocular hypertension and later in 2008 for the treatment of sparse eyelashes, as eyelash growth is considered an ideal side effect for patients using the drug. Bimatoprost is a prostaglandin analog. Bimatoprost is a synthetic prostaglandin amide and structural prostaglandin analog with the ability to lower intraocular pressure. Bimatoprost mimics the action of endogenous prostaglandin amides, lowering intraocular pressure by increasing aqueous humor outflow. Its pathways of action include pressure-sensitive aqueous humor outflow (trabecular meshwork) and pressure-insensitive aqueous humor outflow (uveal-scleral pathway). It is currently unclear whether bimatoprost lowers intraocular pressure by stimulating F-prostaglandin receptors or by acting on specific prostaglandin amide receptors. Bimatoprost is a cloprostol-derived amide drug used as an antihypertensive agent to treat open-angle glaucoma and ocular hypertension. Indications: Bimatoprost is used to lower intraocular pressure in patients with open-angle glaucoma or ocular hypertension. These patients must be intolerant to other intraocular pressure-lowering drugs or have a poor response to other treatments. Bimatoprost is also indicated for the treatment of sparse eyelashes. Lowering intraocular pressure in patients with chronic open-angle glaucoma and ocular hypertension (can be used as monotherapy or in combination with beta-blockers). Treatment of Glaucoma, Treatment of Non-Scarring Alopecia
Treatment of Androgenetic Alopecia
Mechanism of Action
Bimatoprost mimics the action of prostaglandins, particularly prostaglandin F2α. Bimatoprost can mildly stimulate aqueous humor outflow, thereby lowering intraocular pressure and reducing the risk of optic nerve damage. It is believed that bimatoprost lowers intraocular pressure (IOP) in the human eye by increasing the outflow of aqueous humor through the trabecular meshwork and uveal-scleral pathway. It achieves this effect by reducing the resistance to aqueous humor outflow. Bimatoprost does not affect aqueous humor production.
Pharmacodynamics
High intraocular pressure is a major risk factor for glaucoma-related visual field defects. There is a linear relationship between IOP and the risk of optic nerve damage, which can lead to severe visual impairment. Therefore, diseases such as high intraocular pressure and glaucoma can increase the risk of IOP. Bimatoprost can rapidly lower IOP and reduce the risk of visual field defects caused by high intraocular pressure from various causes. Other effects of this drug may include gradual changes in eyelid pigmentation, iris pigmentation, eyelash pigmentation, and eyelash growth and thickening. Patients should be informed of these potential effects, especially when using the drug in only one eye, as bimatoprost treatment may result in noticeable changes in the appearance of the eye.

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Bimaprost (AGN 192024) is a synthetic prostaglandin F2α analog with high selectivity for FP receptors [1, 3, 7].
- Its mechanism of action in lowering intraocular pressure is through activation of FP receptor-mediated signaling pathways (cAMP and Ca2+ pathways) to increase aqueous humor outflow via the trabecular meshwork and uveal-scleral pathways [3, 4, 5].
- Clinically, it is indicated for the treatment of open-angle glaucoma and ocular hypertension to lower intraocular pressure, and for the treatment of sparse eyelashes to promote eyelash growth [1, 7].
- Due to its high affinity for receptors and prolonged duration of ocular action, equiprost has a higher intraocular pressure-lowering efficacy and a longer duration of action compared to other prostaglandin analogues. Duration of stay [6]

C25H37NO4

415.57

415.272

C, 72.26; H, 8.97; N, 3.37; O, 15.40

155206-00-1

5,6-trans-Bimatoprost; 1163135-95-2; Bimatoprost-d5; Bimatoprost methyl ester; 38315-47-8; N-Desethyl Bimatoprost; 155205-89-3; Bimatoprost-d4

5311027

White to off-white solid powder

1.1±0.1 g/cm3

629.8±55.0 °C at 760 mmHg

66-68°C

334.7±31.5 °C

0.0±1.9 mmHg at 25°C

1.591

1.98

4

4

12

30

541

5

O([H])[C@]1([H])C([H])([H])[C@]([H])([C@@]([H])(/C(/[H])=C(\[H])/C([H])(C([H])([H])C([H])([H])C2C([H])=C([H])C([H])=C([H])C=2[H])O[H])[C@]1([H])C([H])([H])/C(/[H])=C(/[H])\C([H])([H])C([H])([H])C([H])([H])C(N([H])C([H])([H])C([H])([H])[H])=O)O[H]

AQOKCDNYWBIDND-FTOWTWDKSA-N

InChI=1S/C25H37NO4/c1-2-26-25(30)13-9-4-3-8-12-21-22(24(29)18-23(21)28)17-16-20(27)15-14-19-10-6-5-7-11-19/h3,5-8,10-11,16-17,20-24,27-29H,2,4,9,12-15,18H2,1H3,(H,26,30)/b8-3-,17-16+/t20-,21+,22+,23-,24+/m0/s1

(Z)-7-[(1R,2R,3R,5S)-3,5-dihydroxy-2-[(E,3S)-3-hydroxy-5-phenylpent-1-enyl]cyclopentyl]-N-ethylhept-5-enamide

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)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.02 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.02 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
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.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.02 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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