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]
\nC57BL/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.\n

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\n\nExperimental procedure and cangrelor administration [2]
\nAccording 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.\n

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\nMice 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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\n\nAssessment of platelet CD62P levels by flow cytometry [3]
\nTo 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 intravenous administration of [3H]cangrelor, 58% of the radioactive material was recovered in the urine. The remaining 35% was in the feces, presumably excreted via bile. In a study of healthy volunteers, administration of a 30 mcg/kg bolus dose followed by a continuous infusion of 4 mcg/kg/min resulted in a volume of distribution of 3.9 L. The mean clearance was approximately 43.2 L/h. /Breast Milk/ It is unclear whether cangrelor is excreted into human breast milk. Following intravenous administration of 3(H)cangrelor, 58% of the radioactive material was recovered in the urine. The remaining 35% was in the feces, presumably excreted via bile. The mean elimination half-life of cangrelor is approximately 3–6 minutes. In a study of healthy volunteers, cangrarel, administered via a bolus dose of 30 μg/kg followed by a continuous infusion of 4 mcg/kg/min, had a volume of distribution of 3.9 L. The plasma protein binding rate of cangrarel is approximately 97-98%. Metabolism/Metabolites Cangrarel is rapidly inactivated in circulation via dephosphorylation to its main metabolite—a nucleoside—which has negligible antiplatelet activity. The metabolism of cangrarel is independent of hepatic function and does not interfere with other drugs metabolized by hepatic enzymes. Biological Half-Life The mean elimination half-life of cangrarel is approximately 3-6 minutes.
After intravenous injection of 3(H) kengril, the elimination half-life of kengril is approximately 3–6 minutes.

Toxicity Summary
Identification and Uses: Cangrelor is a platelet aggregation inhibitor and a purinergic P2Y12 receptor antagonist. Human Studies: Cangrelor is a potent intravenous platelet P2Y12 receptor antagonist with rapid onset and failure. In patients undergoing percutaneous coronary intervention (PCI), compared to controls, Cangrelor (30 μg/kg bolus followed immediately by continuous infusion at a rate of 4 μg/kg/min for 2–4 hours or until the end of the PCI procedure, whichever is longer) reduced the incidence of perioperative thrombotic complications without increasing the incidence of major bleeding complications, but increased the incidence of minor bleeding. In a large Khellinical trial of PCI patients, Cangrelor overdose was rare and not associated with an increase in bleeding complications, possibly due to its very short half-life and rapid failure mechanism of action. Patients with type 2 diabetes mellitus exhibit significantly elevated expression of the platelet P2Y12 receptor, with persistent activation of this receptor. This leads to platelet hyperactivity and limits the efficacy of antiplatelet drugs in type 2 diabetes. Genetic toxicology studies (including the human peripheral blood lymphocyte chromosome aberration assay) have shown that Cangrelor is neither mutagenic nor chromosomal breakage-inducing. Animal studies: After 28 days of treatment with Cangrelor, there was no significant effect on fertility or early embryonic development in either male or female rats. In rat embryo-fetal development studies, Cangrelor caused dose-dependent fetal growth retardation, characterized by an increased incidence of incomplete ossification and unossified metatarsals in the hind limbs. In rabbits, Cangrelor was associated with an increased incidence of abortion and intrauterine loss, as well as fetal growth retardation. In genetic toxicology studies, including in vitro bacterial gene mutation assays, mouse lymphoma thymidine kinase assays, and mouse in vivo bone marrow micronucleus assays, Cangrelor did not demonstrate mutagenicity or chromosomal breakage-inducing properties.

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Hepatotoxicity
In several large Khellinical trials, the incidence of elevated serum ALT in the Cangrelor treatment group was not higher than that in the placebo group [9% vs 12%] or the control group [6.6% vs 6.8%], and no cases of Khellinically significant liver injury with jaundice were reported. Furthermore, since its market launch, there have been no published reports of Khellinically significant liver injury or jaundice caused by Cangrelor treatment, and hepatotoxicity is not mentioned on the product label.
Probability Score: E (Unlikely to cause Khellinically significant liver injury).

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Protein Binding Rate
Approximately 97-98%.

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Interactions
Background: Currently, drugs such as clopidogrel are used to treat patients with cardiovascular disease, while drugs such as Cangrelor and prasugrel are under development; both can act as antagonists of the platelet P2Y12 ADP receptor.
Cangrelor is a direct-acting, reversible antagonist currently under development for short-term infusion; clopidogrel and prasugrel are oral prodrugs that exert irreversible inhibitory effects by transiently forming active metabolites. After discontinuation of Cangrelor infusion, patients typically receive clopidogrel or prasugrel to maintain antiplatelet therapy. Objective: To investigate, using in vitro methods, whether Cangrelor affects the ability of clopidogrel and prasugrel's active metabolites to inhibit ADP-mediated platelet function. Methods: The effects of Cangrelor, clopidogrel (C-AM), and prasugrel (P-AM) active metabolites on platelet function were assessed by detecting ADP-induced platelet P-selectin expression in whole blood. This method included rapid removal of the antagonists through dilution and measurement of residual platelet inhibition. Results: Cangrelor, C-AM, and P-AM all significantly inhibited P-selectin expression. The inhibitory effect of Cangrelor was reversible upon removal of the antagonists, while the inhibitory effects of C-AM and P-AM were irreversible. Pre-incubation of blood with Cangrelor before adding C-AM or P-AM reduces the irreversible antagonistic effect of the metabolite against P2Y12. Pre-incubation of blood with the metabolite before adding Cangrelor maintains this irreversible inhibitory effect. Conclusion: Cangrelor affects the ability of the active metabolites of clopidogrel or prasugrel to irreversibly inhibit platelet function. The timing of oral P2Y12 antagonist administration should be carefully considered after Cangrelor infusion. Concomitant use of Cangrelor with thienopyridine antiplatelet drugs clopidogrel or prasugrel reduces the antiplatelet effect of clopidogrel and prasugrel by blocking the binding of their active metabolites to the P2Y12 receptor. Clopidogrel or prasugrel should not be given orally for maintenance antiplatelet therapy before discontinuing Cangrelor infusion.

[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 analog with the chemical name 5'-O-[({[dichloro(phosphono)methyl](hydroxy)phosphono}oxy)(hydroxy)phosphono]adenosine, with 2-(methylthio)ethyl and (3,3,3-trifluoropropyl)thio substituents at the N6 and C2 positions, respectively. It (in tetrasodium form) is used as an intravenously administered antiplatelet drug to prevent the formation of harmful thrombi in the coronary arteries. It inhibits platelet aggregation and antagonizes P2Y12 receptors. Cangrelor is a nucleoside triphosphate analog, an organofluorine compound, an aryl sulfide, an organochlorine compound, a secondary amino compound, and an adenosine 5'-phosphate ester. It is the conjugate acid of Cangrelor (4-). Cangrelor is an intravenously administered, direct-acting, reversible P2Y12 inhibitor indicated for patients undergoing percutaneous coronary intervention (PCI) who have not yet received oral P2Y12 inhibitors. Compared to oral P2Y12 inhibitors (such as prasugrel, ticagrelor, and clopidogrel), Cangrelor has the advantage of being an active drug that does not require metabolic conversion, resulting in rapid onset and deterioration. Cangrelor was approved by the FDA for intravenous administration in June 2015. Cangrelor is a P2Y12 platelet inhibitor. Its mechanism of action is as a P2Y12 receptor antagonist. The physiological effect of Cangrelor is achieved by reducing platelet aggregation. Cangrelor is an intravenously administered antiplatelet drug used during cardiac surgery or percutaneous coronary intervention to reduce the risk of myocardial infarction and maintain artery and stent patency. Cangrelor has not been found to be associated with serum enzyme abnormalities or Khellinically significant liver injury, but its Khellinical application is limited. Cangrelor is an inhibitor of the platelet adenosine diphosphate (ADP) P2Y12 receptor (P2Y12R) and has antiplatelet activity. Following administration, Cangrelor selectively and reversibly binds to P2Y12R and blocks platelet signaling pathways. This product inhibits the activation of glycoprotein complexes GPIIb/IIIa, fibrinogen binding to platelets, and platelet adhesion and aggregation.

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Indications
For adjunctive treatment of percutaneous coronary intervention (PCI) to reduce the risk of perioperative myocardial infarction (MI), repeat coronary revascularization, and in-stent thrombosis (ST) in patients who have not received P2Y12 platelet inhibitor therapy and are currently not receiving glycoprotein IIb/IIIa inhibitor therapy.
FDA Label
Kengrexal, in combination with acetylsalicylic acid (ASA), is indicated for the reduction of the risk of thrombotic cardiovascular events in adult patients with coronary artery disease undergoing percutaneous coronary intervention (PCI). These patients had not received oral P2Y12 inhibitor therapy prior to PCI, and oral P2Y12 inhibitor therapy was not feasible. Ideal.

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Mechanism of Action
Cangrelor is a selective, reversible P2Y12 platelet receptor antagonist that inhibits ADP-induced platelet aggregation. ADP is normally released from damaged blood vessels, erythrocytes, and/or platelets upon agonist stimulation, thereby promoting platelet activity. ADP binds to P2Y12, inhibiting adenylate cyclase via Gi protein, thereby stimulating and completing platelet aggregation, which in turn enhances the secretion of dense granules and improves coagulation activity. Cangrelor has the same target and mechanism of action as the oral irreversible inhibitors clopidogrel and ticlopidine, but its effect is reversible, with a rapid onset and failure rate.
Cangrelor is a direct P2Y12 platelet receptor inhibitor that blocks ADP-induced platelet activation and aggregation. Cangrelor selectively and reversibly binds to the P2Y12 receptor, thereby blocking further signaling and platelet activation.

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Therapeutic Use
Platelet aggregation inhibitor; Purinergic P2Y receptor antagonist
/Khellinical Trials/ KhellinicalTrials.gov is a registry and outcomes database that indexes human Khellinical studies funded by public and private institutions worldwide. This website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on KhellinicalTrials.gov provides a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure under investigation); the study title, description, and design; 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). Cangrelor is indexed in this database.
Cangrelor is indicated as adjunctive therapy for percutaneous coronary intervention (PCI) to reduce the risk of perioperative myocardial infarction (MI), repeat coronary revascularization, and stent thrombosis in patients who have not received P2Y12 platelet inhibitor therapy or glycoprotein IIb/IIIa inhibitor therapy. /Included on US product label/

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Drug Warnings
The most common adverse reaction reported in Khellinical trials of Cangrelor is bleeding. Transient dyspnea has also been reported during Khellinical trials.
Hypersensitivity reactions (e.g., anaphylactic shock, bronchospasm, angioedema, wheezing) have been reported with Cangrelor treatment.
As with other antiplatelet drugs, Cangrelor increases the risk of bleeding, and bleeding can be severe. In the CHAMPION PHOENIX trial, the incidence of bleeding events of all severities was slightly higher in the Cangrelor group than in the clopidogrel group. In Khellinical trials, bleeding events in patients treated with Cangrelor were generally mild, typically manifesting as hematoma, ecchymosis, and oozing at the puncture site. In the CHAMPION PHOENIX trial, Cangrelor did not significantly increase the incidence of major bleeding according to the Global Opening and Closing Coronary Artery Strategy [GUSTO] criteria; however, according to the more sensitive criteria (Acute Catheter Insertion and Emergency Triage Strategy [ACUITY]), the incidence of major bleeding was significantly higher in the Cangrelor group than in the clopidogrel group (4.3% vs. 2.5%). According to the ACUITY criteria, the increased incidence of major bleeding was attributed to a higher incidence of hematoma at the vascular access site in patients treated with Cangrelor. Cangrelor should not be used in patients with significant active bleeding. The antiplatelet effect of Cangrelor is negligible 1 hour after infusion cessation. For more complete data on drug warnings for Cangrelor (11 in total), please visit the HSDB record page. Cangrelor tetrasodium is an organic sodium salt, the tetrasodium salt of Cangrelor. It is an intravenously administered antiplatelet drug that prevents the formation of harmful thrombi in the coronary arteries. It inhibits platelet aggregation and antagonizes the P2Y12 receptor. It contains the Cangrelor (4-) molecule. Cangrelor tetrasodium is the tetrasodium form of Cangrelor, a platelet adenosine diphosphate (ADP) P2Y12 receptor (P2Y12R) inhibitor with antiplatelet activity. After administration, Cangrelor selectively and reversibly binds to P2Y12R and blocks the platelet signaling pathway. This product inhibits the activation of glycoprotein complexes GPIIb/IIIa, the binding of fibrinogen to platelets, and platelet adhesion and aggregation.

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Drug Indications
Kengrexal, in combination with acetylsalicylic acid (ASA), is indicated for adult patients with coronary artery disease undergoing percutaneous coronary intervention (PCI) who have not received oral P2Y12 inhibitor therapy prior to PCI, or whose oral P2Y12 inhibitor therapy is not feasible or appropriate, but can be used to reduce the incidence of thrombotic cardiovascular events after PCI.
As more and more patients with cardiovascular and neurological diseases receive antiplatelet therapy, perioperative management of these patients can be challenging. Preventing ischemia and thrombosis is crucial, while reducing the risk of bleeding; therefore, effective bridging therapy is needed.
Cangrelor has unique pharmacokinetic characteristics, rapid onset of action, and easy reversibility, making it a promising bridging therapy option. However, large prospective studies are still needed to develop clear guidelines, identify which patient populations will benefit most from antiplatelet bridging therapy, determine optimal dosage and titration regimens, monitor treatment efficacy, and manage adverse events. Although guidelines recommend intravenous bridging therapy in these cases, no drug has been approved by the FDA for this indication, and there is a lack of positive randomized controlled data on glycoprotein IIb/IIIa inhibitors (GPIs) in this indication. The advantage of Cangrelor bridging therapy is that it has a faster onset of action and is not cleared by the kidneys, so it seems to be superior to the standard therapy that previously used GPIs. Future research is needed to explore the use of Cangrelor in special populations, such as patients with coronary artery disease (CAD) receiving dual antiplatelet therapy (DAPT), as a bridging therapy for left ventricular assist device (LVAD) implantation. In conclusion, in today's rapidly evolving medical technology, therapies like Cangrelor have the potential to reduce the risk of perioperative thrombosis and bleeding. [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.)