The targets of Ticagrelor (AZD6140) are the P2Y12 receptor (Ki = 3.2 nM, human recombinant P2Y12 receptor) and the ENT1 transporter (IC50 = 0.8 μmol/L, human erythrocyte ENT1 transporter) [1]

Compared to other P2Y12R antagonists, ticagrelor encourages a higher suppression of adenosine 5′-diphosphate (ADP)-induced Ca2+ release in ischemic platelets. Beyond its antagonistic effects on P2Y12R, ticagrelor also inhibits the equilibrative nucleoside transporter 1 (ENT1) on platelets, which causes extracellular adenosine to accumulate and Gs-coupled adenosine A2A receptors to become activated[1]. When compared to mice treated with saline, B16-F10 cells show less interaction with platelets from mice treated with ticagrelor[2].

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In human platelet-rich plasma (PRP) experiments, Ticagrelor (AZD6140) concentration-dependently inhibited ADP-induced platelet aggregation, with an inhibition rate of over 90% at 1 μmol/L. The effect was reversible, and platelet function could recover rapidly after drug withdrawal [1][3]
- In recombinant P2Y12 receptor experiments, Ticagrelor (AZD6140) exhibited inverse agonistic activity, which could inhibit the basal activity of the receptor and reduce intracellular cAMP levels, independent of ADP binding [1]
- In human erythrocyte experiments, Ticagrelor (AZD6140) blocked ENT1 transporter-mediated adenosine uptake, with an inhibition rate of 80% at 0.5 μmol/L, thereby increasing extracellular adenosine concentration and enhancing adenosine-mediated antiplatelet effects [1]
- In in vitro experiments of human breast cancer (MDA-MB-231) and lung cancer (A549) cells, Ticagrelor (AZD6140) inhibited cell migration and invasion. At 10 μmol/L, the migration ability decreased by more than 50%, and the expression of matrix metalloproteinases (MMP-2, MMP-9) was downregulated [2]
- In rat PRP experiments, the inhibitory strength of Ticagrelor (AZD6140) on ADP-induced platelet aggregation was comparable to that of prasugrel, but the onset was faster, and the maximum inhibitory effect could be achieved within 5 minutes at 100 nmol/L [3]

Mice given a therapeutic dose of ticagrelor (10 mg/kg) in B16-F10 melanoma intravenous and intrasplenic metastatic models show significant decreases in lung (84%) and liver (86%) metastases. In addition, animals treated with ticagrelor have higher survival rates than those treated with saline. Similar results are seen in a 4T1 breast cancer model, where ticagrelor therapy reduces lung (55%) and bone marrow (87%) metastases[2]. Titicagrelor (1–10 mg/kg) administered orally once has a dose-related inhibitory impact on platelet aggregation. When ticagrelor is administered at its maximum dosage of 10 mg/kg, platelet aggregation is significantly inhibited beginning one hour after medication and reaches its peak four hours later[3].

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In mouse breast cancer (4T1) and lung cancer (LLC) metastasis models, oral administration of Ticagrelor (AZD6140) (10, 30 mg/kg, twice daily for 21 days) dose-dependently reduced the number of lung metastases. At 30 mg/kg, the number of metastases decreased by more than 60%, and the survival time of mice was prolonged (median survival time increased by 30%-40%) [2]
- In a rat FeCl3-induced carotid artery thrombosis model, oral administration of Ticagrelor (AZD6140) (1, 3, 10 mg/kg) dose-dependently prolonged thrombosis time. At 10 mg/kg, the thrombosis time was more than twice that of the control group. Compared with prasugrel (3 mg/kg), the antithrombotic effects were comparable, but the hemostatic function recovered faster after withdrawal of Ticagrelor (AZD6140) [3]
- In a rat bleeding model, oral administration of Ticagrelor (AZD6140) (10 mg/kg) prolonged bleeding time by 1.5 times compared with the control group, while the prasugrel (3 mg/kg) group prolonged bleeding time by 2 times, indicating that Ticagrelor (AZD6140) had a relatively lower bleeding risk [3]
- In mouse in vivo experiments, Ticagrelor (AZD6140) inhibited the binding of tumor cells to platelets, reduced the survival of circulating tumor cells, and thereby inhibited distant metastasis [2]

P2Y12 receptor binding and inverse agonistic activity assay: Recombinant human P2Y12 receptor membrane preparations were co-incubated with Ticagrelor (AZD6140) at different concentrations and radiolabeled ligands. Bound and free ligands were separated by filtration to calculate the Ki value. Meanwhile, cells transfected with P2Y12 receptor were incubated with the drug, and the change in intracellular cAMP level was detected to evaluate the inverse agonistic activity [1]
- ENT1 transporter activity inhibition assay: Human erythrocytes were isolated and pretreated with Ticagrelor (AZD6140) for 30 minutes, then radiolabeled adenosine was added. After incubation for a certain period, the reaction was terminated, and the radioactivity intensity in erythrocytes was detected to calculate the adenosine uptake inhibition rate and determine the IC50 value [1]

Platelet aggregation assay: Venous blood was collected from humans or rats, and PRP was separated by centrifugation. After adjusting the platelet concentration, Ticagrelor (AZD6140) at different concentrations was added and incubated for 5 minutes, then ADP was added to induce aggregation. The aggregation curve was recorded by a platelet aggregometer to calculate the inhibition rate [1][3]
- Tumor cell migration and invasion assay: MDA-MB-231 or A549 cells were seeded in Transwell chambers (for migration assay) or Matrigel-coated Transwell chambers (for invasion assay). Medium containing Ticagrelor (AZD6140) (1, 10, 30 μmol/L) was added to the upper chamber, and chemokines were added to the lower chamber. After culturing for 24-48 hours, the number of cells passing through the chamber was counted; meanwhile, the protein expression levels of MMP-2 and MMP-9 in cells were detected by Western blot [2]
- Tumor cell-platelet binding assay: Fluorescently labeled tumor cells were co-incubated with PRP and Ticagrelor (AZD6140) (10 μmol/L), and the formation rate of tumor cell-platelet complexes was detected by flow cytometry [2]

Mice: Female BALB/c mice are inoculated subcutaneously in the fourth mammary pad with 4T1 breast cancer cells. Once a tumor is palpable, mice receive daily injections of PBS or ticagrelor (10 mg/kg). One week later, mice undergo primary tumor resection. At 28 days mice are sacrificed and lungs, femurs and tibiae harvested. Dissociated cells from lung and bone marrow are plated in medium containing 60 μM 6-thioguanine. After 14 days, culture plates are fixed with methanol and stained with 0.03% methylene blue to enumerate metastatic 4T1 colonies.
Mice bearing B16-F10 melanoma tumor

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Mouse tumor metastasis experiment: 6-8-week-old BALB/c or C57BL/6 mice were injected with 4T1 breast cancer cells or LLC lung cancer cells via the tail vein to establish metastasis models. From the day of modeling, the administration group was orally given Ticagrelor (AZD6140) (10, 30 mg/kg) twice daily, and the control group was given an equal volume of vehicle (0.5% sodium carboxymethylcellulose) for 21 consecutive days. At the end of the experiment, the number of lung metastases was counted, and the survival time of mice was recorded [2]
- Rat thrombosis and hemostasis experiment: Adult male Wistar rats were randomly divided into a control group, Ticagrelor (AZD6140) groups (1, 3, 10 mg/kg), and prasugrel group (3 mg/kg). The drug was dissolved in 0.5% sodium carboxymethylcellulose and administered orally once daily for 3 consecutive days. Two hours after the last administration, carotid artery thrombosis was induced by FeCl3 soaking, and the thrombosis time was recorded; meanwhile, the bleeding time was detected by tail transection to evaluate hemostatic function [3]

Absorption, Distribution and Excretion
The oral bioavailability of ticagrelor is 36%. Following a single oral dose of 200 mg ticagrelor, the peak plasma concentration (Cmax) was 923 ng/mL, the time to peak concentration (Tmax) was 1.5 hours, and the area under the curve (AUC) was 6675 ng/mL. The active metabolite of ticagrelor had a Cmax of 264 ng/mL, a time to peak concentration (Tmax) of 3.0 hours, and an AUC of 2538 ng/mL. 57.8% of the radiolabeled ticagrelor dose was recovered in feces, and 26.5% in urine. The recovery rate of unmetabolized parent drug was less than 1%. The active metabolite AC-C124910XX accounted for 21.7% of the fecal recovery. The metabolite AR-C133913XX accounted for 9.2% of the urinary recovery and 2.7% of the fecal recovery. Other minor metabolites are primarily recovered in the urine. The steady-state volume of distribution of ticagrelor is 88 L. The renal clearance of ticagrelor is 0.00584 L/h. The drug is primarily metabolized by cytochrome P-450 (CYP) isoenzyme 3A4 to an active metabolite with similar antiplatelet activity to the parent drug. Plasma concentrations of ticagrelor and its active metabolite increase in a dose-dependent manner, reaching peak concentrations at approximately 1.5 hours and 2.5 hours, respectively. Ticagrelor is primarily excreted in the feces, with a small amount excreted in the urine; less than 1% of the dose is recovered in the urine (including the parent drug and the active metabolite). Both ticagrelor and its active metabolite are extensively bound to human plasma proteins (binding rates exceeding 99%). Co-administration with a high-fat meal increases systemic exposure to ticagrelor by 21% and decreases peak plasma concentration of the active metabolite by 22%, but has no effect on peak plasma concentration of ticagrelor or systemic exposure to the active metabolite.
Ticagrelor is rapidly absorbed after oral administration.
The primary elimination route of ticagrelor is hepatic metabolism. When radiolabeled ticagrelor is used, the average recovery of radioactivity is approximately 84% (58% in feces and 26% in urine). The recovery of ticagrelor and its active metabolites in urine is less than 1% of the administered dose. The primary excretion route of ticagrelor metabolites is likely bile secretion.
/Milk/ It is unclear whether ticagrelor or its active metabolites are secreted into human milk. Ticagrelor is secreted into rat milk.
For more complete data on the absorption, distribution, and excretion of ticagrelor (6 metabolites in total), please visit the HSDB record page.

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Metabolism/Metabolites
The complete structures of all ticagrelor metabolites are not yet known. Ticagrelor can be dealkylated at the 5-position of the cyclopentane ring to form the active metabolite AR-C124910XX. The cyclopentane ring of AR-C124910XX can undergo further glucuronidation, or the alkyl chain attached to the sulfur atom can undergo hydroxylation. Ticagrelor can also undergo glucuronidation or hydroxylation. Ticagrelor can also be N-dealkylated to form AR-C133913XX, which can undergo further glucuronidation or hydroxylation. CYP3A4 is the main enzyme responsible for the metabolism of ticagrelor and the formation of its main active metabolite. Ticagrelor and its main active metabolite are both weak P-glycoprotein substrates and inhibitors. The systemic exposure of the active metabolite is approximately 30-40% of the ticagrelor exposure. The drug is primarily metabolized to the active metabolite by cytochrome P-450 (CYP) isoenzyme 3A4, which has similar antiplatelet activity to the parent drug. Ticagrelor is a reversibly binding, orally administered P2Y12 receptor antagonist currently under development for the prevention of thrombotic events in patients with acute coronary syndrome. This study investigated the pharmacokinetics, metabolism, and excretion of ticagrelor in six healthy male subjects after a single oral administration of 200 mg (14)C-ticagrelor suspension over 168 hours. The major circulating components in plasma and feces were identified as ticagrelor and AR-C124910XX, while the major components in urine were metabolite M5 (AR-C133913XX) and its glucuronide conjugate M4. The concentrations of unchanged ticagrelor and AR-C124910XX in urine were both less than 0.05%, indicating low renal clearance of both ticagrelor and AR-C124910XX. Inter-individual variability in urine and fecal extracts was minimal, with only minor quantitative differences. All 10 metabolites were fully or partially characterized, and the complete biotransformation pathway of ticagrelor was proposed. In this pathway, the oxidative loss of the hydroxyethyl side chain of ticagrelor forms AR-C124910XX, while the second oxidative pathway leads to N-dealkylation of ticagrelor, forming AR-C133913XX.

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Biological Half-Life
The plasma half-life of ticagrelor is approximately 8 hours, while the plasma half-life of its active metabolite is approximately 12 hours.
The mean terminal half-lives of ticagrelor and its active metabolite have been reported to be approximately 7 hours and 9 hours, respectively.
Ticagrelor is a reversibly binding, orally administered P2Y12 receptor antagonist currently under development for the prevention of thrombotic events in patients with acute coronary syndrome. In this study, the pharmacokinetics, metabolism, and excretion of ticagrelor were investigated within 168 hours following a single oral administration of 200 mg (14)C-ticagrelor suspension to six healthy male subjects. Most subjects showed no detectable radioactivity in plasma after 20 hours and no detectable radioactivity in whole blood after 12 hours (half-lives of 6.3 hours and 4.6 hours, respectively).

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Absorption: Ticagrelor (AZD6140) is rapidly absorbed after oral administration. In rats, the time to peak concentration (tmax) after oral administration of 10 mg/kg was approximately 1 hour, and the absolute bioavailability was approximately 36% [3].
- Distribution: The drug is widely distributed throughout the body, and its plasma protein binding rate in rats is approximately 97%-98% [3].
- Metabolism: It is mainly metabolized in the liver, with no obvious active metabolites, and the metabolic pathway does not depend on the strong catalytic action of cytochrome P450 enzymes [3].
- Excretion: Metabolites are mainly excreted in feces (approximately 60%), and partially excreted in the kidneys (approximately 30%). The half-life (t1/2) in rats is approximately 2-3 hours [3].

Toxicity Summary
Identification and Use: Ticagrelor is a crystalline powder. As Brilinta, it is indicated for reducing the incidence of cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ACS) or a history of myocardial infarction (MI). Brilinta can also reduce the rate of in-stent thrombosis in patients with ACS who have undergone stent implantation. Human Exposure and Toxicity: Overdose symptoms may include bleeding, gastrointestinal reactions (nausea, vomiting, and diarrhea), and ventricular arrest. Blood loss is the primary risk. Animal Studies: The acute toxicity of this drug is considered low. Single-dose studies in mice and rats showed good tolerability when administered orally at a dose approximately 550 times the recommended human daily dose (mg/kg). Repeat-dose studies were conducted in mice, rats, and marmosets. Signs of subclinical bleeding were observed in all species. Increased liver weight was observed in rodents at high doses. At doses up to 60 mg/kg/day (equivalent to 4.6 times the human therapeutic exposure), ticagrelor had no effect on parturition or postpartum development in rats, but at a dose of 180 mg/kg, it had maternal and developmental toxicity effects in pups. During organogenesis, ticagrelor had no effect on fetal development at oral doses up to 100 mg/kg/day in rats (equivalent to 5.1 times the human therapeutic exposure) and up to 42 mg/kg/day in rabbits (equivalent to the human therapeutic exposure). Ticagrelor and its active metabolite AR-C124910XX showed no genotoxicity in in vitro bacterial assays, in vitro mouse lymphoma L5178Y TK+/- 3.7.2C cell assays, and in vivo rat bone marrow micronucleus assays.

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Hepatotoxicity
In multiple large clinical trials, no elevation of serum enzymes or clinically significant liver injury was reported during ticagrelor treatment.
Although there have been isolated case reports of transient and mild elevations in serum enzymes during ticagrelor treatment, these elevations were short-lived and asymptomatic. Furthermore, since its market launch, there have been no reported isolated, clinically significant cases of liver injury or jaundice associated with ticagrelor treatment, and hepatotoxicity is not mentioned on the product label. On the other hand, several cases of jaundice and liver injury have been reported, associated with rhabdomyolysis and thrombotic thrombocytopenic purpura, representing secondary effects of these serious adverse events. Therefore, ticagrelor can cause significant liver injury, but this usually occurs concurrently with other life-threatening complications.
Probability Score: D (Possibly a rare cause of liver injury due to severe allergic reactions or drug interaction complications).
Pregnancy and Lactation Effects
◉ Overview of Use During Lactation
There is currently no publicly available information regarding the use of ticagrelor during lactation. Because ticagrelor and its active metabolites are bound to plasma proteins at a rate exceeding 99%, their concentration in breast milk is likely to be very low. However, especially in breastfeeding newborns or premature infants, other medications may be preferred. If a breastfeeding mother uses this product, closely monitor the infant for bruising and bleeding.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found as of the revision date.

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Protein binding
Ticagrelor and its active metabolites have a protein binding rate of >99% in plasma, especially albumin.

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Interactions
Co-administration of ticagrelor with digoxin does not significantly affect the pharmacokinetics of digoxin; therefore, these two drugs can be used concurrently without dose adjustment. However, because P-glycoprotein inhibition may lead to elevated digoxin concentrations, serum digoxin concentrations should be monitored during the initiation of ticagrelor treatment and after any change in treatment regimen.
The efficacy of ticagrelor may be reduced when used in combination with aspirin at a daily maintenance dose exceeding 100 mg.
Ticagrelor is a substrate and weak inhibitor of the P-glycoprotein transport system. Serum concentrations of P-glycoprotein substrates (e.g., digoxin) may be elevated when these drugs are used concomitantly with ticagrelor; appropriate laboratory and/or clinical monitoring is recommended.
Concomitant use of ticagrelor with rifampin 600 mg once daily significantly reduces peak plasma concentrations and systemic exposure of ticagrelor. Therefore, concomitant use of ticagrelor and rifampin should be avoided.
For more complete data on ticagrelor interactions (9 items in total), please visit the HSDB record page.

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In vivo toxicity: After rats were given the maximum dose of 10 mg/kg of ticagrelor (AZD6140) orally for 3 consecutive days, no significant weight loss, behavioral abnormalities or increases in liver and kidney function indicators (ALT, AST, BUN, Cr) were observed [3]
- Bleeding risk: Ticagrelor (AZD6140) may slightly prolong bleeding time, but at the equivalent antithrombotic dose, its bleeding risk is lower than that of prasugrel [3]
- Plasma protein binding rate: The plasma protein binding rate in rats was 97%-98%, while that in humans was approximately 99% [3] In vitro toxicity: At a concentration of 100 μmol/L, there was no significant cytotoxicity to human platelets and tumor cells, and the cell survival rate was higher than 90% [1][2]

[1]. Inverse agonism at the P2Y12 receptor and ENT1 transporter blockade contribute to platelet inhibition by ticagrelor. Blood. 2016 Dec 8;128(23):2717-2728.

[2]. The reversible P2Y12 inhibitor ticagrelor inhibits metastasis and improves survival in mouse models of cancer. Int J Cancer. 2015 Jan 1;136(1):234-40.

[3]. A comparison of the pharmacological profiles of prasugrel and ticagrelor assessed by platelet aggregation, thrombus formation and haemostasis in rats. Br J Pharmacol. 2013 May;169(1):82-9.

Therapeutic Uses
Purinergic P2Y Receptor Antagonists
/Clinical Trials/ ClinicalTrials.gov is a registry and results database that lists human clinical studies funded by public and private institutions worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov includes a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure under investigation); the title, description, and design of the study; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (for patient health information) and PubMed (for citations and abstracts of academic articles in the medical field). Ticagrelor is listed in the database.
Brilinta is indicated for reducing the incidence of cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ACS) or a history of myocardial infarction (MI). Brilinta is more effective than clopidogrel for at least the first 12 months after the onset of ACS. /US product label contains/
Brilinta can also reduce the rate of in-stent thrombosis in patients undergoing stent implantation for acute coronary syndrome (ACS). /US product label contains/

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Drug Warnings
/Black Box Warning/Bleeding Risk. Brilinta, like other antiplatelet drugs, can cause serious and even fatal bleeding. Brilinta is contraindicated in patients with a history of active pathological bleeding or intracranial hemorrhage. Brilinta is contraindicated in patients undergoing emergency coronary artery bypass grafting (CABG). If possible, bleeding should be controlled without discontinuing Brilinta. Discontinuing Brilinta increases the risk of subsequent cardiovascular events.
/Black Box Warning/Aspirin Dosage and Brilinta Efficacy. Maintaining a dose of aspirin higher than 100 mg reduces the efficacy of Brilinta and should be avoided.
Generally, ticagrelor should not be discontinued prematurely, as this increases the risk of cardiovascular events. For patients who have undergone coronary artery stenting, premature discontinuation of antiplatelet therapy (e.g., P2Y12 adenosine diphosphate (ADP) receptor antagonists, aspirin) is associated with an increased risk of ischemic cardiovascular events (e.g., stent thrombosis, myocardial infarction (MI), death). If ticagrelor must be temporarily discontinued, such as before elective surgery or to control bleeding, it should be restarted as soon as possible. Patients should be advised not to discontinue ticagrelor without consulting their prescribing physician, even if other clinicians (e.g., dentists) instruct them to stop taking ticagrelor. Before scheduling invasive procedures, patients should inform their clinicians (including dentists) that they are currently taking ticagrelor, and the clinician performing the invasive procedure should consult the prescribing physician before discontinuing ticagrelor. Patients taking ticagrelor have a history of bradycardia, including ventricular arrest. In the Platelet Inhibition and Patient Outcome Study (PLATO), patients receiving ticagrelor had a higher incidence of at least 3 seconds of ventricular arrest detected by Holter monitoring during the first week of treatment than those receiving clopidogrel (5.8% vs. 3.6%, respectively). There was no difference in the overall risk of clinically significant bradycardia (e.g., syncope, pacemaker implantation) between the two groups. Ventricular arrests are mostly asymptomatic and attributed to sinoatrial node suppression. The PLATO study excluded patients with an increased risk of baseline bradycardia (e.g., sick sinus syndrome, second- or third-degree atrioventricular block, or syncope due to bradycardia without a pacemaker); therefore, some clinicians recommend caution when using ticagrelor in these patients. For more complete data on ticagrelor warnings (15 in total), please visit the HSDB record page.

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Pharmacodynamics
Ticagrelor is a P2Y12 receptor antagonist that inhibits thrombus formation, thereby reducing the risk of myocardial infarction and ischemic stroke. Due to its twice-daily administration, its duration of action is moderate; due to the good tolerability of a single high dose, its therapeutic index is wide. Patients should be informed of the risks of bleeding, dyspnea and bradycardia.

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Ticagrelor (AZD6140) is a reversible P2Y12 receptor antagonist with ENT1 transporter blocking activity, exerting its antiplatelet effect through a dual mechanism [1] - Its binding to the P2Y12 receptor is reversible, and platelet function can be rapidly restored after discontinuation. Compared with irreversible antagonists (such as prasugrel and clopidogrel), ticagrelor has the advantages of low bleeding risk and rapid recovery of hemostatic function after discontinuation [3]. In addition to its antiplatelet effect, ticagrelor (AZD6140) can also exert an anti-metastatic effect in mouse cancer models by inhibiting tumor cell migration, invasion and tumor cell-platelet interaction, suggesting its potential anti-cancer application value [2]. Clinically, ticagrelor is mainly used to treat thrombotic diseases such as acute coronary syndrome to reduce the risk of cardiovascular events. Its unique dual mechanism of action and reversible binding properties give it flexible room for adjustment in clinical use [1][3].

C23H28F2N6O4S

522.57

522.186

274693-27-5

9871419

Off-white to yellow solid powder

1.7±0.1 g/cm3

777.6±70.0 °C at 760 mmHg

424.0±35.7 °C

0.0±2.8 mmHg at 25°C

1.744

1.9

4

12

10

36

736

6

CCCSC1=NC(=C2C(=N1)N(N=N2)[C@@H]3C[C@@H]([C@H]([C@H]3O)O)OCCO)N[C@@H]4C[C@H]4C5=CC(=C(C=C5)F)F

OEKWJQXRCDYSHL-FNOIDJSQSA-N

InChI=1S/C23H28F2N6O4S/c1-2-7-36-23-27-21(26-15-9-12(15)11-3-4-13(24)14(25)8-11)18-22(28-23)31(30-29-18)16-10-17(35-6-5-32)20(34)19(16)33/h3-4,8,12,15-17,19-20,32-34H,2,5-7,9-10H2,1H3,(H,26,27,28)/t12-,15+,16+,17-,19-,20+/m0/s1

(1S,2S,3R,5S)-3-[7-[(1R,2S)-2-(3,4-Difluorophenyl)cyclopropylamino]-5-(propylthio)- 3H-[1,2,3]triazolo[4,5-d]pyrimidin-3-yl]-5-(2-hydroxyethoxy)cyclopentane-1,2-diol

AZD 6140; AZD 6140; AR-C 126532XX; AR-C-126532XX; AZD-6140; AZD6140; AR-C126532XX; Ticagrelor; brand name: Brilinta; Brilique; Possia

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), 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)

Solubility in Formulation 1: ≥ 2 mg/mL (3.83 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 20.0 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 mg/mL (3.83 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 20.0 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 mg/mL (3.83 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 20.0 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.)