Cangrelor tetrasodium has a pKb of 8.6–9.2 for the hP2Y12 receptor[3]. Tetrasodium Cangeler is the only effective intravenous direct potential adenosine diphosphate (ADP) P2Y12 receptor clamping agent [1]. The hP2Y12 receptor pKb of tetrasodium cangeler is 8.6-9.2 [3].

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Cangrelor is a selective, rapidly reversible P2Y12 platelet receptor inhibitor that directly blocks adenosine diphosphate (ADP)-induced activation and aggregation of platelets and achieves a 90% level of platelet inhibition within five minutes [1].

In addition to dramatically lowering BLM-induced inflammatory cytokine production (PF4, CD40 L, and MPO), cangrelor tetrasodium (10 mg/kg) also decreases peripheral platelets, neutrophils, and platelet-neutrophils, as well as fibrotic lung and platelet-neutrophil accumulation in the blood of BLM-treated mice [2].

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Researchers have reported that cangrelor, a non-sepesific GPR17 antagonist, alleviates pulmonary fibrosis partly by inhibiting macrophage inflammation in mice. Cangrelor is also a well-known anti-platelet agent. To test whether cangrelor mitigated pulmonary fibrosis partly through the inhibition of platelets, bleomycin (BLM) was used to induce pulmonary fibrosis in C57BL/6 J mice. We found that cangrelor (10 mg/kg) not only significantly decreased BLM-induced release of inflammatory cytokines (PF4, CD40 L and MPO), but also decreased the increment of platelets, neutrophils and platelet-neutrophil aggregates in the fibrotic lung and in the peripheral blood of BLM-treated mice. In addition, cangrelor decreased the number of CD40 and MPO double positive neutrophils and the expression level of CD40 in BLM-treated mouse lungs. Based on these results we conclude that cangrelor alleviates BLM-induced lung inflammation and pulmonary fibrosis in mice, partly through inhibition of platelet activation, therefore reducing the infiltration of neutrophils due to the adhesion of platelets and neutrophils mediated by CD40 - CD40 L interaction. Cangrelor could be a potential therapeutic medicine for pulmonary fibrosis. [2]

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Methods Complete Freund's adjuvant (CFA)-induced chronic inflammatory pain was induced in wild-type and P2ry12 gene-deficient (P2ry12-/- ) mice, and the potent, direct-acting and reversible P2Y12 receptor antagonists PSB-0739 and cangrelor were used. Results CFA-induced mechanical hyperalgesia was significantly decreased in P2ry12-/- mice for up to 14 days, and increased neutrophil myeloperoxidase activity and tumor necrosis factor (TNF)-α and CXCL1 (KC) levels in the hind paws were also attenuated in the acute inflammation phase. At day 14, increased interleukin (IL)-1β, IL-6, TNF-α and KC levels were attenuated in P2ry12-/- mice. PSB-0739 and cangrelor reversed hyperalgesia in wild-type mice but had no effect in P2ry12-/- mice, and PSB-0739 was also effective when applied locally. The effects of both local and systemic PSB-0739 were prevented by A-803467, a selective NaV1.8 channel antagonist, suggesting the involvement of NaV1.8 channels in the antihyperalgesic effect. Platelet depletion by anti-mouse CD41 antibody decreased hyperalgesia and attenuated the proinflammatory cytokine response in wild-type but not in P2ry12-/- mice on day 14. Conclusions In conclusion, P2Y12 receptors regulate CFA-induced hyperalgesia and the local inflammatory response, and platelet P2Y12 receptors contribute to these effects in the chronic inflammation phase[3].

Animals and reagents [2]
C57BL/6 J mice (male, 6–8 weeks, 22−25 g) were used. The mice are free access to water and food in air-conditioned rooms (23 °C, relative humidity 50 %) on a 12 h light / dark cycle. Four treatments were performed in these mice: sham-operated control (Con, n = 6), cangrelor (Cang, 10 mg/kg, n = 6), bleomycin + saline (BLM, 3 mg/kg, n = 6) and bleomycin + cangrelor (BLM + Cang 10 mg/kg, n = 6). Cangrelor and bleomycin (Hisun Pharmaceutical Co., Ltd., China) were stored at 4 °C and diluted in saline before use.

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Experimental procedure and cangrelor administration [2]
According to the previous report (Zhan et al., 2018, 2018; Tanaka et al., 2017), pulmonary fibrosis was induced by intratracheal administration of bleomycin (BLM, 3 mg/kg) in C57BL/6 J mice, and cangrelor (10 mg/kg) was administrated via subcutaneous injection. BLM was administrated on day 0, the treatment of cangrelor was started 2 days before BLM administration and lasted for 16 days (once per day). On day 14, the mice were sacrificed by cervical dislocation after the pulmonary resistance was determined. The bronchoalveolar lavage fluid (BALF) was collected from right lung, then the right lung tissues were stored at -80 °C for Western blotting analysis and quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The left lung tissues were fixed in 10 % formaldehyde for histological inspection. The blood and BALF were collected for flow cytometry and ELISA assay.

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Mice were treated with P2Y12R antagonists, or with their vehicle (sterile saline), intraperitoneally ([dichloro‐[[[(2R,3S,4R,5R)‐3,4‐dihydroxy‐5‐[6‐(2‐methylsulfanylethylamino)‐2‐(3,3,3‐trifluoropropylsulfanyl)purin‐9‐yl]oxolan‐2‐yl]methoxy‐hydroxyphosphoryl]‐oxyhydroxyphosphoryl]methyl]phosphonic‐acid, cangrelor , 3 mg kg−1; The Medicines Company, Parsippany, NJ, USA), intraplantarly or intrathecally (1‐amino‐4‐[4‐phenylamino‐3‐sulfophenylamino]‐9,10‐dioxo‐9,10‐dihydroanthracene‐2‐sulfonate, PSB‐0739, 0.3 mg kg−1, selective P2Y12R antagonist synthesized by Y. Baqi and C. E. Müller). on days 3, 4, 7, 10 and 14 after CFA injection. The doses were chosen on the basis of our previous experiments: the pKB values of PSB‐0739 and cangrelor at human P2Y12Rs (hP2Y12Rs) were 9.8 and 8.6, respectively, whereas, in the doses applied in the present study (PSB‐0739, 0.3 mg kg−1 intrathecally; cangrelor , 3 mg kg−1 intraperitoneally), they reversed acute inflammatory pain for up to 96 h. Taking into account that the approximate blood volume of a 25‐mg mice is 1700 μL, these doses correspond to 5 μm and 50 μm, indicating maximal target inhibition. As a reference compound, aspirin, an alternative platelet antagonist, was used at a low dose (2‐acetyloxybenzoic acid, 20 mg kg−1 intraperitoneally). The mechanonociceptive thresholds of hind paws were measured 15 min or 30 min after intrathecal/intraperitoneal or intraplantar injections, with the exception of day 3, when PWT measurements were performed before drug administration. 5‐(4‐chlorophenyl)‐N‐(3,5‐dimethoxyphenyl)‐2‐furancarboxamide (A‐803467, 30 mg kg−1), a potent and selective NaV1.8 sodium channel antagonist or its vehicle (polyethylene glycol and dimethyl sulfoxide [9 : 1]) was administered intraperitoneally 5 min before the respective PSB‐0739/saline injection. The dose of A‐803467 was chosen on the basis of a previous study, and a submaximal dose (30 mg kg−1 intraperitoneally) in the reduction of mechanical allodynia was selected to reveal any additive interactions between PSB‐0739 and A‐803467. In some experiments, paw edema was also volumetrically quantified by plethysmometry (7140; Ugo Basile). [3]

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Assessment of platelet CD62P levels by flow cytometry [3]
To investigate how P2Y12R antagonists and antiplatelet agents administered via different routes altered platelet activation, we measured ADP‐induced changes in platelet CD62P levels ex vivo, in platelet‐rich plasma (PRP) samples. Wild‐type mice were treated with PSB‐0739 (0.3 mg kg−1 intrathecally), cangrelor (3 mg kg−1 intraperitoneally), aspirin (20 mg kg−1 intraperitoneally), or their vehicle. Blood samples were taken directly from the vena cava of anesthetized mice 15 min or 30 min after the treatment. Apyrase (1 U mL−1) was added to the samples to prevent ADP receptor desensitization. After 10 min of centrifugation at 150 × g, PRP was collected. Platelet activation was induced by ADP (500 μm), and changes in platelet CD62P levels were assessed after 60 min of incubation. Platelets were stained with anti‐human/mouse CD62P antibody for 10 min. Samples were acquired with a BD FACSVerse machine, and analyzed with BD facsuite software. Changes in CD62P mean fluorescence intensity values were determined on CD42d‐positive platelets.

Absorption, Distribution and Excretion
Following IV administration of [3H] cangrelor, 58% of radioactivity was recovered in urine. The remaining 35% of radioactivity was in feces, presumably following biliary excretion.
In a study in healthy volunteers administration at a dose of 30 mcg/kg bolus plus 4 mcg/kg/min showed a volume of distribution of 3.9 L.
The mean clearance is about 43.2 L/h.
/MILK/ It is not known whether Kengreal is excreted in human milk.
Following IV administration of 3(H) Kengreal 58% of radioactivity was recovered in urine. The remaining 35% of radioactivity was in feces, presumably following biliary excretion. The average elimination half-life of Kengreal is about 3-6 minutes.
In a study in healthy volunteers, Kengreal administration at a dose of 30 ug/kg bolus plus 4 mcg/kg/min showed a volume of distribution of 3.9 L. Plasma protein binding of Kengreal is about 97-98%.

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Metabolism / Metabolites
Cangrelor is deactivated rapidly in the circulation by dephosphorylation to its primary metabolite, a nucleoside, which has negligible anti-platelet activity. Cangrelor's metabolism is independent of hepatic function and it does not interfere with other drugs metabolized by hepatic enzymes.
Kengreal is deactivated rapidly in the circulation by dephosphorylation to its primary metabolite, a nucleoside, which has negligible anti-platelet activity. Kengreal's metabolism is independent of hepatic function and it does not interfere with other drugs metabolized by hepatic enzymes.

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Biological Half-Life
The average elimination half-life of cangrelor is about 3-6 minutes.
Following IV administration of 3(H) Kengreal, ... elimination half-life of Kengreal is about 3-6 minutes.

Toxicity Summary
IDENTIFICATION AND USE: Cangrelor is a platelet aggregation inhibitor and purinergic P2Y receptor antagonist. HUMAN STUDIES: Cangrelor is a potent intravenous platelet P2Y12 receptor antagonist with rapid onset and offset of action. In patients undergoing percutaneous coronary interventions (PCI), compared with control, cangrelor (30 ug/kg bolus, followed immediately by a 4 ug/kg per minute infusion for 2-4 hr or until the conclusion of the index PCI, whichever was longer) reduces periprocedural thrombotic complications without an increase in major bleeding complications, although minor bleeding is increased. In a large clinical trial program of patients undergoing PCI, cangrelor overdosing was rare and not associated with an increase in bleeding complications, an observation that may be attributed to its very short-half life and rapid offset of action. Platelet P2Y12 receptor expression is significantly increased and the receptor is constitutively activated in patients with type 2 diabetes mellitus, which contributes to platelet hyperactivity and limits antiplatelet drug efficacy in type 2 diabetes mellitus. Cangrelor was non-mutagenic and non-clastogenic in genetic toxicology studies, including chromosome aberration assay in human peripheral lymphocytes. ANIMAL STUDIES: Cangrelor had no significant effect on male or female rats fertility treated for 28 days, or on early embryonic development. In embryo-fetal development studies in rats, cangrelor produced dose-related fetal growth retardation characterized by increased incidences of incomplete ossification and unossified hind limb metatarsals. In rabbits, cangrelor was associated with increased incidences of abortion and intrauterine losses, as well as fetal growth retardation. Cangrelor was non-mutagenic and non-clastogenic in genetic toxicology studies, including in vitro bacterial gene mutation assay, mouse lymphoma thymidine kinase assay, and in vivo bone marrow micronucleus assay in mice.

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Hepatotoxicity
In several large clinical trials, serum ALT elevations were no more frequent with cangrelor therapy than with placebo [9% vs 12%] or with comparator arms [6.6% vs 6.8%] and no cases of clinically apparent liver injury with jaundice were reported. In addition, since marketing and release, there have been no published reports of clinically apparent liver injury or jaundice associated with cangrelor therapy and hepatotoxicity is not mentioned in the product label.
Likelihood score: E (unlikely cause of clinically apparent liver injury).

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Protein Binding
about 97-98%.

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Interactions
BACKGROUND: Agents that act as antagonists at P2Y(12) ADP receptors on platelets are in use (clopidogrel), and in development for use (cangrelor and prasugrel), in patients with cardiovascular disease. Cangrelor is a direct-acting reversible antagonist being developed for short-term infusion; clopidogrel and prasugrel are oral prodrugs that provide irreversible inhibition via transient formation of active metabolites. At the cessation of cangrelor infusion, patients are likely to receive clopidogrel or prasugrel as a means of maintaining antiplatelet therapy. OBJECTIVES: To apply an experimental in vitro approach to investigate the possibility that cangrelor influences the ability of the active metabolites of clopidogrel and prasugrel to inhibit ADP-mediated platelet function. METHODS: The effects of cangrelor and the active metabolites of clopidogrel (C-AM) and prasugrel (P-AM) on platelet function were assessed by ADP-induced platelet P-selectin expression in whole blood. The method involved rapid removal of the antagonists by dilution, and measurement of residual platelet inhibition. RESULTS: Cangrelor, C-AM and P-AM markedly inhibited P-selectin expression. The effect of cangrelor, but not of C-AM and P-AM, was reversible following antagonist removal. Preincubation of blood with cangrelor prior to addition of C-AM or P-AM reduced the ability of metabolites to irreversibly antagonize P2Y(12). Irreversible inhibition was maintained when blood was preincubated with metabolites prior to cangrelor. CONCLUSIONS: Cangrelor influences the ability of the active metabolites of clopidogrel or prasugrel to inhibit platelet function irreversibly. Careful consideration should be given to the timing of administration of an oral P2Y(12) antagonist following cangrelor infusion.
Concomitant administration of cangrelor with the thienopyridine antiplatelet drugs clopidogrel or prasugrel decreases the antiplatelet effect of clopidogrel and prasugrel by blocking P2Y12-receptor binding of the active metabolites of these drugs. Oral maintenance antiplatelet therapy with clopidogrel or prasugrel should not be administered until the cangrelor infusion has been discontinued.

[1]. Intravenous cangrelor as a peri-procedural bridge with applied uses in ischemic events. Ann Transl Med. 2019;7(17):408.

[2]. Cangrelor alleviates bleomycin-induced pulmonary fibrosis by inhibiting platelet activation in mice. Mol Immunol. 2020;120:83-92.

[3]. Contribution of platelet P2Y12 receptors to chronic Complete Freund's adjuvant-induced inflammatory pain. J Thromb Haemost. 2017;15(6):1223-1235.

Cangrelor is a nucleoside triphosphate analogue that is 5'-O-[({[dichloro(phosphono)methyl](hydroxy)phosphoryl}oxy)(hydroxy)phosphoryl]adenosine carrying additional 2-(methylsulfanyl)ethyl and (3,3,3-trifluoropropyl)sulfanyl substituents at positions N6 and C2 respectively. Used (in the form of its tetrasodium salt) as an intravenous antiplatelet drug that prevents formation of harmful blood clots in the coronary arteries. It has a role as a platelet aggregation inhibitor and a P2Y12 receptor antagonist. It is a nucleoside triphosphate analogue, an organofluorine compound, an aryl sulfide, an organochlorine compound, a secondary amino compound and an adenosine 5'-phosphate. It is a conjugate acid of a cangrelor(4-).
Cangrelor is an intravenous, direct-acting, reversible P2Y12 inhibitor for patients undergoing percutaneous coronary intervention (PCI) who have not been yet treated by oral P2Y12 inhibitors. An advantage Cangrelor provides over oral P2Y12 inhibitors (such as prasugrel, ticagrelor, and clopidogrel) is that it is an active drug not requiring metabolic conversion therefore providing a rapid onset and offset of action. Cangrelor was approved by the FDA in June 2015 for intravenous application.
Cangrelor is a P2Y12 Platelet Inhibitor. The mechanism of action of cangrelor is as a P2Y12 Receptor Antagonist. The physiologic effect of cangrelor is by means of Decreased Platelet Aggregation.
Cangrelor is an intravenously administered antiplatelet drug that is used at the time of cardiac surgery or percutaneous coronary intervention to decrease the risk of myocardial infarction and maintain artery and stent patency. Cangrelor has not been linked to serum enzyme abnormalities or to clinically apparent liver injury, but its clinical use has been limited.
Cangrelor is an inhibitor of the platelet adenosine diphosphate (ADP) P2Y12 receptor (P2Y12R), with antiplatelet activity. Upon administration, cangrelor selectively and reversibly binds to P2Y12R, and blocks the platelet signaling pathway. This inhibits the activation of the glycoprotein complex GPIIb/IIIa, fibrinogen binding to platelets and platelet adhesion and aggregation.

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Drug Indication
For use as an adjunct to percutaneous coronary intervention (PCI) for reducing the risk of periprocedural myocardial infarction (MI), repeat coronary revascularization, and stent thrombosis (ST) in patients in who have not been treated with a P2Y12 platelet inhibitor and are not being given a glycoprotein IIb/IIIa inhibitor.
FDA Label
Kengrexal, co-administered with acetylsalicylic acid (ASA), is indicated for the reduction of thrombotic cardiovascular events in adult patients with coronary artery disease undergoing percutaneous coronary intervention (PCI) who have not received an oral P2Y12 inhibitor prior to the PCI procedure and in whom oral therapy with P2Y12 inhibitors is not feasible or desirable.

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Mechanism of Action
Cangrelor is a selective, reversible, P2Y12 platelet receptor antagonist which inhibits ADP platelet aggregation. ADP is typically released by damaged blood vessels, red blood cells, and/or platelets due to agonists stimulating platelet activity. ADP binds to P2Y12 to stimulate and complete platelet aggregation by inhibiting adenylyl cyclase by a Gi protein, thus potentiating dense granule secretion and increasing coagulation activity. Cangrelor acts on the same target as oral irreversible inhibitors clopidogrel and ticlopidine and has a similar mechanism of action, but is reversible and provides a fast onset and offset of action.
Cangrelor is a direct P2Y12 platelet receptor inhibitor that blocks ADP-induced platelet activation and aggregation. Cangrelor binds selectively and reversibly to the P2Y12 receptor to prevent further signaling and platelet activation.

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Therapeutic Uses
Platelet Aggregation Inhibitors; Purinergic P2Y Receptor Antagonists
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Cangrelor is included in the database.
Kengreal is indicated as an adjunct to percutaneous coronary intervention (PCI) to reduce the risk of periprocedural myocardial infarction (MI), repeat coronary revascularization, and stent thrombosis (ST) in patients who have not been treated with a P2Y12 platelet inhibitor and are not being given a glycoprotein IIb/IIIa inhibitor. /Included in US product label/

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Drug Warnings
The most common adverse effect of cangrelor reported in clinical trials was bleeding. Cases of transient dyspnea were also reported during clinical trials.
Hypersensitivity reactions (e.g., anaphylaxis, bronchospasm, angioedema, stridor) have been reported with cangrelor therapy.
Like other antiplatelet agents, cangrelor increases the risk of bleeding, which may be serious. In the CHAMPION PHOENIX trial, bleeding events of all severities were somewhat more common with cangrelor than with clopidogrel. In clinical trials, bleeding events in patients receiving cangrelor were mild, generally consisting of hematoma, ecchymosis, and oozing at the puncture site. In the CHAMPION PHOENIX trial, the rate of severe bleeding (per the Global Use of Strategies to Open Occluded Coronary Arteries [GUSTO] criteria) was not substantially increased by cangrelor, although the rate of major bleeding according to more sensitive criteria (Acute Catheterization and Urgent Intervention Triage Strategy [ACUITY]) was substantially higher with cangrelor than with clopidogrel (4.3 versus 2.5%). The increase in major bleeding with the ACUITY criteria was attributable to a greater incidence of hematoma at the site of vascular access in patients receiving cangrelor.
Cangrelor should not be used in patients with substantial active bleeding. The antiplatelet effects of cangrelor are negligible 1 hour after discontinuance of the infusion.
For more Drug Warnings (Complete) data for Cangrelor (11 total), please visit the HSDB record page.

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Cangrelor tetrasodium is an organic sodium salt that is the tetrasodium salt of cangrelor. Used as an intravenous antiplatelet drug that prevents formation of harmful blood clots in the coronary arteries. It has a role as a platelet aggregation inhibitor and a P2Y12 receptor antagonist. It contains a cangrelor(4-).
Cangrelor Tetrasodium is the tetrasodium salt form of cangrelor, an inhibitor of the platelet adenosine diphosphate (ADP) P2Y12 receptor (P2Y12R), with antiplatelet activity. Upon administration, cangrelor selectively and reversibly binds to P2Y12R, and blocks the platelet signaling pathway. This inhibits the activation of the glycoprotein complex GPIIb/IIIa, fibrinogen binding to platelets and platelet adhesion and aggregation.

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Drug Indication
Kengrexal, co-administered with acetylsalicylic acid (ASA), is indicated for the reduction of thrombotic cardiovascular events in adult patients with coronary artery disease undergoing percutaneous coronary intervention (PCI) who have not received an oral P2Y12 inhibitor prior to the PCI procedure and in whom oral therapy with P2Y12 inhibitors is not feasible or desirable.

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Due to the increasing number of patients on antiplatelet therapy for cardiovascular and neurological conditions, it can be challenging to manage these patients peri-operatively. It is critical to prevent ischemia and thrombosis, and at the same time decrease the risk of bleeding, necessitating the need for a successful bridging therapy. Cangrelor looks promising as a bridging therapy with its distinctive pharmacokinetic profile with fast activity and easy reversibility. However, large prospective studies are required to delineate clear guidelines to identify the patient population that would receive maximum benefit from bridging antiplatelet therapy, determine optimal dosing and titration, monitoring therapy, and manage adverse events. Although guidelines recommend IV bridge therapy in these settings, no agent currently has FDA-approval for this indication and positive, randomized controlled data for GPIs in this setting is also lacking. Cangrelor bridging therapy appears to have advantages over the previous standard using GPIs due to its faster offset and non-renal clearance. Future research is warranted for use of cangrelor in special populations, such as those with CAD on DAPT as a bridge to LVAD implantation. Overall, in this complex era of advancing medical technologies, therapies such as cangrelor may mitigate thrombotic and bleeding risks in the peri-operative period. [1]

C24H27N3O4S

776.359300000001

774.948

C, 26.30; H, 3.25; Cl, 9.13; F, 7.34; N, 9.02; O, 24.73; P, 11.97; S, 8.26

163706-06-7

Cangrelor tetrasodium;163706-36-3

9854012

Typically exists as solid at room temperature

2.087g/cm3

979.004ºC at 760 mmHg

545.882ºC

0mmHg at 25°C

1.722

2.923

7

21

15

44

1140

4

CSCCNC1=C2C(=NC(=N1)SCCC(F)(F)F)N(C=N2)[C@H]3[C@@H]([C@@H]([C@@H](COP(=O)(O)OP(=O)(C(Cl)(Cl)P(=O)(O)O)O)O3)O)O

PAEBIVWUMLRPSK-IDTAVKCVSA-N

InChI=1S/C17H25Cl2F3N5O12P3S2/c1-43-5-3-23-12-9-13(26-15(25-12)44-4-2-16(20,21)22)27(7-24-9)14-11(29)10(28)8(38-14)6-37-42(35,36)39-41(33,34)17(18,19)40(30,31)32/h7-8,10-11,14,28-29H,2-6H2,1H3,(H,33,34)(H,35,36)(H,23,25,26)(H2,30,31,32)/t8-,10-,11-,14-/m1/s1

(dichloro((((((2R,3S,4R,5R)-3,4-dihydroxy-5-(6-((2-(methylthio)ethyl)amino)-2-((3,3,3-trifluoropropyl)thio)-9H-purin-9-yl)tetrahydrofuran-2-yl)methoxy)(hydroxy)phosphoryl)oxy)(hydroxy)phosphoryl)methyl)phosphonic acid

AR-C69931; AR C69931; MXAR C69931; 163706-06-7; Kengreal; AR-C69931XX; Cangrelor free acid; UNII-6AQ1Y404U7; 6AQ1Y404U7; ARL69931; AR-C69931MX; ARC69931MX; ARC69931

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)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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