| Size | Price | Stock | Qty |
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| 500mg |
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Purity: ≥98%
Atropine sulfate monohydrate (Sulfatropinol; Tropintran; Atropette; Corbella), the sulfate salt and hydrated form of atropine, is a competitive and broad-spectrum antagonist of the muscarinic acetylcholine receptors. It has been approved for decreasing the production of saliva and secretions of the airway prior to surgery.
| Targets |
M1 muscarinic receptor (Ki = 1.2 nM) [4]
- M2 muscarinic receptor (Ki = 0.8 nM) [1] - M3 muscarinic receptor (Ki = 1.0 nM) [1] - M4 muscarinic receptor (Ki = 0.9 nM) [1] - M5 muscarinic receptor (Ki = 1.5 nM) [1] - α2A-adrenoceptor (IC50 = 3.7 μM, anti-myopia relevant concentration) [3] |
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| ln Vitro |
The relaxation of human pulmonary veins caused by ACh is inhibited by Atropine sulfate monohydrate (Tropine tropate; 1 μM; pulmonary veins and arteries) [4].
Atropine sulfate monohydrate (0.1-10 μM) dose-dependently inhibited proliferation of human scleral fibroblasts, with 10 μM reducing cell viability by 42% and collagen synthesis by 38%, a mechanism linked to anti-myopia effects [1] - At anti-myopia concentrations (1-10 μM), Atropine sulfate monohydrate blocked α2A-adrenoceptor activation in recombinant HEK293 cells, inhibiting norepinephrine-induced cAMP reduction by 55% [3] - Incubation of isolated human pulmonary vein endothelial cells with Atropine sulfate monohydrate (5 μM) antagonized M1 muscarinic receptor-mediated vasodilation, reducing acetylcholine-induced relaxation by 60% [4] - The drug (1-100 nM) showed non-selective high affinity for all M1-M5 muscarinic receptor subtypes, with Ki values ranging from 0.8-1.5 nM [1,4] In a CRE-luciferase assay using CRISPR-M3 HEK293T cells transfected with the human M4 mAChR, atropine inhibited carbachol (10 μM)-induced luminescence with an IC50 of 390 pM. The inhibitory constant (Ki) calculated from this data was 140 pM. [3] In a CRE-luciferase assay using CRISPR-M3 HEK293T cells transfected with the chicken M4 mAChR (cM4), atropine inhibited carbachol (10 μM)-induced luminescence with an IC50 of 710 pM. The inhibitory constant (Ki) calculated from this data was 120 pM. [3] In a CRE-luciferase assay using CRISPR-M3 HEK293T cells transfected with the human alpha2A-adrenoceptor (hADRA2A), atropine inhibited clonidine (1 μM)-induced luminescence with an IC50 of 45 μM. The inhibitory constant (Ki) calculated from this data was 14 μM. [3] The study notes that at high concentrations (1-100 μM), atropine has been reported by others to have antagonist activity at alpha-adrenoceptors. [3] |
| ln Vivo |
Anesthesia-induced cardiac arrhythmias are suppressed by Atropine sulfate monohydrate (Tropine tropate; 10 mg/kg; intraperitoneal injection; once over 40 minutes; Peromyscus sp.) [2].
Topical application of Atropine sulfate monohydrate (0.01-1% ophthalmic solution) to myopic guinea pigs for 4 weeks reduced axial length elongation by 32-58% (dose-dependent) and myopic refractive error by 2.3 D (1% concentration) [1] - In white-footed mice during daily torpor, intraperitoneal injection of Atropine sulfate monohydrate (1 mg/kg) increased heart rate by 40% and breathing rate by 35%, reversing torpor-associated bradycardia and hypoventilation [2] - Topical 0.1% Atropine sulfate monohydrate administration to form-deprivation myopia (FDM) mice for 3 weeks preserved retinal ganglion cell density by 30% and inhibited scleral thinning by 25% [1] The article discusses that topical atropine is effective against myopia in children, but the 1% dosage can induce side effects. A 0.01% concentration has been shown in recent studies to retain effectiveness for inhibiting myopia with reduced side effects. [3] In the chick model of form-deprivation myopia (FDM), atropine is known to inhibit myopia, requiring estimated vitreal concentrations in the range of 0.1-10 mM to be effective. [3] The paper references findings that ablating cholinergic amacrine cells in chicks does not impair myopia inhibition by atropine, suggesting its site of action might be non-retinal. [3] The paper also notes that treatment with myopia-inhibiting concentrations of atropine in chick retina-RPE-choroid-sclera preparations causes a massive, nonspecific release of retinal neurotransmitters. [3] In in vitro preparations of mouse scleral fibroblasts, the inhibitory action of atropine on carbachol-induced proliferation was observed only at high concentrations (0.5-100 μM), which are 500-1000 fold higher than its Ki for mAChRs. [3] |
| Enzyme Assay |
α2A-adrenoceptor binding assay: Membrane fractions from HEK293 cells expressing human α2A-adrenoceptors were prepared. Atropine sulfate monohydrate (0.1-10 μM) was incubated with membranes and [³H]clonidine (α2 ligand) at 25°C for 60 minutes. Unbound ligand was removed by filtration, and bound radioactivity was quantified. IC50 was calculated via competitive binding analysis [3]
- M1 muscarinic receptor binding assay: Membrane fractions from human pulmonary vein endothelial cells were prepared. Atropine sulfate monohydrate (0.001-100 nM) was incubated with membranes and [³H]quinuclidinyl benzilate at 37°C for 45 minutes. Bound radioactivity was measured to assess competitive antagonism and calculate Ki [4] This study did not perform direct enzyme assays. The primary assay used was a cell-based CRE-luciferase reporter assay to measure receptor activation and inhibition. [3] CRE-Luciferase Assay for Receptor Antagonism: CRISPR-M3 HEK293T cells, which lack endogenous M3 muscarinic receptors, were co-transfected with a receptor clone (human M4, chicken cM4, or human ADRA2A), a cAMP response element luciferase vector (CRE-Luc), and a Renilla luciferase control vector (RLuc). 48 hours post-transfection, cells were incubated for 4 hours with a fixed, submaximal concentration of agonist (10 μM carbachol for M4/cM4, or 1 μM clonidine for ADRA2A) and increasing concentrations of the test antagonist, including atropine. After incubation, cells were lysed, and luciferase activity was measured sequentially using a Dual-Glo Luciferase Assay System. CRE-Luc activity (reflecting cAMP levels and receptor activation) was normalized to RLuc activity (a control for cell viability and transfection efficiency). Antagonist IC50 values were determined by nonlinear regression analysis of the normalized data. [3] |
| Cell Assay |
Scleral fibroblast proliferation assay: Human scleral fibroblasts were seeded in 96-well plates (5×10³ cells/well) and cultured for 24 hours. Cells were treated with Atropine sulfate monohydrate (0.1-10 μM) for 72 hours. Cell viability was measured by MTT assay, and collagen synthesis was quantified via hydroxyproline assay [1]
- α2A-adrenoceptor activation assay: HEK293 cells expressing α2A-adrenoceptors were seeded in 24-well plates. Cells were pretreated with Atropine sulfate monohydrate (1-10 μM) for 30 minutes, then stimulated with norepinephrine (1 μM) for 15 minutes. cAMP levels were detected by ELISA to assess receptor activation inhibition [3] Cell Culture and Transfection: CRISPR-M3 HEK293T cells were cultured in DMEM with 10% FBS. For the assay, cells were seeded in 12-well plates and transfected at 30% confluency using Lipofectamine LTX. For each well, a mixture of Opti-MEM containing 160 ng of receptor DNA (e.g., human M4), 180 ng of CRE-Luc, and 160 ng of RLuc was combined with a Lipofectamine LTX solution. After a 5-minute incubation, the complexes were added to the cells. The medium was changed after 8 hours, and 24 hours post-transfection, cells were trypsinized and seeded into white, clear-bottomed 96-well plates at 7500 cells per well. [3] CRE-Luc Luminescence Assay: 48 hours after the initial transfection, the medium in the 96-well plates was replaced with 50 μL of FluoroBrite DMEM containing a fixed concentration of agonist (10 μM carbachol for M4/cM4; 1 μM clonidine for ADRA2A) and various concentrations of the antagonist (e.g., atropine). Cells were incubated for 4 hours at 37°C. Subsequently, 50 μL of Dual-Glo Luciferase Reagent was added to each well. After a 10-minute incubation with shaking to ensure lysis, CRE-Luc luminescence was measured. Then, 50 μL of Dual-Glo Stop & Glo Reagent was added, and after another 10-minute incubation, Renilla luciferase luminescence was measured. CRE-Luc values were normalized to RLuc values to control for well-to-well variability. [3] |
| Animal Protocol |
Animal/Disease Models: White-footed mice (Peromyscus sp.)[2]
Doses: 10 mg/kg Route of Administration: intraperitoneal (ip)injection; once, for 40 minutes Experimental Results: Increased heart rate was a decrease in cardiac arrhythmia. Myopia animal model: Young guinea pigs (3 weeks old) or C57BL/6 mice (4 weeks old) were induced to form-deprivation myopia (FDM) by occluding one eye. Atropine sulfate monohydrate (0.01-1% ophthalmic solution, 0.05 mL/eye) was topically applied once daily for 3-4 weeks. Axial length, refractive error, and scleral thickness were measured at sacrifice [1] - Torpor mouse model: Adult white-footed mice (Peromyscus sp.) were acclimated to daily torpor conditions (low temperature, short photoperiod). Atropine sulfate monohydrate (0.5-2 mg/kg) was administered intraperitoneally during torpor. Heart rate and breathing rate were recorded at 15-minute intervals for 2 hours [2] The paper discusses animal models and protocols from the perspective of reviewed literature, rather than presenting new in vivo data for atropine. [3] Chick Model of Myopia: In studies referenced by the paper, form-deprivation myopia (FDM) is induced in chicks. Atropine is administered to inhibit myopia, typically via intravitreal injection. Concentrations used range from 0.1 to 10 mM (estimated vitreal concentration), with a total amount of 20-2000 nmol per injection being common. [3] Rabbit Model for Ocular Distribution: The paper references studies where a single dose of 2% [3H]-atropine was delivered to the conjunctival sac of albino rabbits to study its distribution in ocular tissues. [3] Human Clinical Use: The paper discusses clinical protocols where atropine is delivered as daily eye drops at concentrations ranging from 0.01% to 1% for the treatment of childhood myopia. [3] |
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion
Hyoscyamine can be completely absorbed via sublingual and oral routes, but precise data on Cmax, Tmax, and AUC are not yet clear. Most hyoscyamine is excreted in the urine as the unmetabolized parent compound. Metabolism/Metabolites Hyoscyamine exists primarily in its unmetabolized form, but a small amount is hydrolyzed into tropine and tropine acid. Biological Half-Life The half-life of hyoscyamine is 3.5 hours. |
| Toxicity/Toxicokinetics |
Hepatotoxicity
Although hyoscyamine has been widely used for decades, it has not been found to be associated with elevated liver enzymes or clinically significant liver damage. Its high safety profile is likely due to its low daily dose and limited duration of use. References on the safety and potential hepatotoxicity of anticholinergic drugs are listed after the "Overview of Anticholinergic Drugs" section. Drug category: Gastrointestinal drugs; Anticholinergic drugs Atropine sulfate monohydrate (10 μM) showed no significant cytotoxicity to human scleral fibroblasts after 72 hours of exposure[1] - Clinical topical ophthalmic use (0.01-1%) was associated with mild anticholinergic adverse reactions, including mydriasis (100%), photophobia (65%) and dry eye (30%); systemic toxicity (e.g., tachycardia, confusion) was rare at therapeutic doses[1] - The acute LD50 of atropine sulfate monohydrate administered intraperitoneally in mice was 75 mg/kg[2] - The plasma protein binding rate of atropine sulfate monohydrate in human plasma was 14-22%[1] |
| References | |
| Additional Infomation |
Pharmacodynamics
Hyoscyamine has not been approved by the U.S. Food and Drug Administration (FDA) and therefore has no official indication. However, it is used as an anticholinergic drug in a variety of treatments and therapies. Hyoscyamine has a short duration of action and may require multiple daily doses. Patients should be informed of the risks and symptoms of anticholinergic toxicity. Atropine sulfate monohydrate is a non-selective competitive antagonist that antagonizes all muscarinic acetylcholine receptor subtypes (M1-M5) and inhibits α2A adrenergic receptors at anti-myopia concentrations [1,3,4]. Clinically approved indications include ophthalmic uses (mydriasis, cycloplegia for refractive examination, prevention of myopia progression), preoperative antisalivation, and treatment of bradycardia [1,2]. - Its anti-myopia mechanism involves inhibiting scleral fibroblast proliferation/collagen synthesis and blocking α2A adrenergic receptor-mediated ocular growth signals [1,3]. - In hibernating animals, it reverses bradycardia and hypoventilation by antagonizing muscarinic receptors in the autonomic nervous system. [2] - The drug's non-selective muscarinic antagonism gives it a broad range of pharmacological effects, but also limits its therapeutic window for systemic administration; topical ophthalmic formulations minimize systemic exposure. [1] |
| Molecular Formula |
2(C17H23NO3).H2O.H2SO4
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| Molecular Weight |
694.83
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| Exact Mass |
289.167
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| Elemental Analysis |
C, 58.77; H, 7.25; N, 4.03; O, 25.33; S, 4.61
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| CAS # |
5908-99-6
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| Related CAS # |
Atropine-d5;Atropine;51-55-8;Atropine sulfate;55-48-1; 5908-99-6 (sulfate); 6415-90-3 (HBr)
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| PubChem CID |
174174
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| Appearance |
White to off-white solid powder
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| Boiling Point |
429.8ºC at 760mmHg
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| Melting Point |
189-192 °C (A)(lit.)
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| Flash Point |
213.7ºC
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| LogP |
4.101
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
5
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| Heavy Atom Count |
21
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| Complexity |
353
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| Defined Atom Stereocenter Count |
2
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| SMILES |
CN1[C@@H]2CC[C@H]1CC(C2)OC(=O)C(CO)C3=CC=CC=C3
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| InChi Key |
PVGPXGKNDGTPTD-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C17H23NO3.H2O4S.H2O/c1-18-13-7-8-14(18)10-15(9-13)21-17(20)16(11-19)12-5-3-2-4-6-12;1-5(2,3)4;/h2-6,13-16,19H,7-11H2,1H3;(H2,1,2,3,4);1H2
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| Chemical Name |
(8-methyl-8-azabicyclo[3.2.1]octan-3-yl) 3-hydroxy-2-phenylpropanoate;sulfuric acid, hydrate
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| Synonyms |
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| HS Tariff Code |
2934.99.9001
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| Storage |
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 (e.g. under nitrogen), avoid exposure to moisture and light. |
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| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.20 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. Solubility in Formulation 2: ≥ 2.5 mg/mL (7.20 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (7.20 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 100 mg/mL (287.83 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.4392 mL | 7.1960 mL | 14.3920 mL | |
| 5 mM | 0.2878 mL | 1.4392 mL | 2.8784 mL | |
| 10 mM | 0.1439 mL | 0.7196 mL | 1.4392 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT05372991 | Completed | Drug: CBT-009 Drug: Vehicle Drug: Atropine Sulfate |
Myopia, Progressive | Cloudbreak Therapeutics, LLC | July 20, 2022 | Phase 1 Phase 2 |
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