TICAGRELOR

Details

Stereochemistry	ABSOLUTE
Molecular Formula	C23H28F2N6O4S
Molecular Weight	522.568
Optical Activity	UNSPECIFIED
Defined Stereocenters	6 / 6
E/Z Centers	0
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

CCCSC1=NC2=C(N=NN2[C@@H]3C[C@H](OCCO)[C@@H](O)[C@H]3O)C(N[C@@H]4C[C@H]4C5=CC=C(F)C(F)=C5)=N1

InChI

InChIKey=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

HIDE SMILES / InChI

Molecular Formula	C23H28F2N6O4S
Molecular Weight	522.568
Charge	0
Count

Stereochemistry	ABSOLUTE
Additional Stereochemistry	No
Defined Stereocenters	6 / 6
E/Z Centers	0
Optical Activity	UNSPECIFIED

Description
Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/022433s015lbl.pdf
Curator's Comment: description was created based on several sources, including http://www.ema.europa.eu/docs/en_GB/document_library/PIP_decision/WC500123240.pdf; http://www.ema.europa.eu/docs/en_GB/document_library/EPAR_-_Summary_for_the_public/human/002303/WC500100562.pdf; https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf

Ticagrelor (known trade names Brilinta, Brilique and Possia) is a P2Y12 platelet inhibitor. Brilinta has been approved by the US Food and Drug administration (FDA) in 2011 and is indicated to reduce the rate of cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ACS) or a history of myocardial infarction. Brilinta also reduces the rate of stent thrombosis in patients who have been stented for treatment of ACS. Ticagrelor and its major metabolite reversibly interact with the platelet P2Y12 ADP-receptor to prevent signal transduction and platelet activation. Ticagrelor and its active metabolite are approximately equipotent. In vitro metabolism studies demonstrate that ticagrelor and its major active metabolite are weak inhibitors of CYP3A4, potential activators of CYP3A5 and inhibitors of the P-gp transporter. Most common adverse reactions are bleeding 12% and dyspnea 14%.

Originator

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
Purinergic receptor P2Y12 23 Target ID: CHEMBL2001 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/022433s015lbl.pdf	Antagonist 2778

Conditions

Condition	Modality	Targets	Highest Phase	Product
Acute coronary syndrome 33 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/022433s015lbl.pdf	Secondary		Approved 8429	BRILINTA Approved Use Indicated to reduce the rate of cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ACS) or a history of myocardial infarction (MI). For at least the first 12 months following ACS, it is superior to clopidogrel. Reduces the rate of stent thrombosis in patients who have been stented for treatment of ACS. Launch Date 2011
Myocardial infarction 121 Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2015/022433s015lbl.pdf	Secondary		Approved 8429	BRILINTA Approved Use Indicated to reduce the rate of cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome (ACS) or a history of myocardial infarction (MI). For at least the first 12 months following ACS, it is superior to clopidogrel. Reduces the rate of stent thrombosis in patients who have been stented for treatment of ACS. Launch Date 2011

C_max

Value	Dose	Analyte	Population
1583 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/20642549/	200 mg 2 times / day multiple, oral dose: 200 mg route of administration: Oral experiment type: MULTIPLE co-administered:	TICAGRELOR plasma	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED
1208 ng/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT01898442	270 mg single, oral dose: 270 mg route of administration: oral experiment type: single co-administered:	TICAGRELOR plasma	Homo sapiens
1208 ng/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT01898442	360 mg single, oral dose: 360 mg route of administration: oral experiment type: single co-administered:	TICAGRELOR plasma	Homo sapiens

AUC

Value	Dose	Analyte	Population
10160 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/20642549/	200 mg 2 times / day multiple, oral dose: 200 mg route of administration: Oral experiment type: MULTIPLE co-administered:	TICAGRELOR plasma	Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED
12379 ng*h/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT01898442	270 mg single, oral dose: 270 mg route of administration: oral experiment type: single co-administered:	TICAGRELOR plasma	Homo sapiens
12381 ng*h/mL Clinical Trial https://clinicaltrials.gov/ct2/show/NCT01898442	360 mg single, oral dose: 360 mg route of administration: oral experiment type: single co-administered:	TICAGRELOR plasma	Homo sapiens

T_1/2

Value	Dose	Co-administered	Analyte	Population
7 h DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/022433s028lbl.pdf	90 mg single, oral dose: 90 mg route of administration: Oral experiment type: SINGLE co-administered:		TICAGRELOR plasma	Homo sapiens population: UNKNOWN age: ADULT sex: FEMALE / MALE food status: UNKNOWN

F_unbound

Value	Dose	Co-administered	Analyte	Population
1% DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/022433s028lbl.pdf	90 mg single, oral dose: 90 mg route of administration: Oral experiment type: SINGLE co-administered:		TICAGRELOR plasma	Homo sapiens population: UNKNOWN age: ADULT sex: FEMALE / MALE food status: UNKNOWN

Doses

Dose	Population	Adverse events
1260 mg single, oral Highest studied dose Dose: 1260 mg Route: oral Route: single Dose: 1260 mg Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	healthy n = 6 Health Status: healthy Population Size: 6 Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	DLT: Gastrointestinal disorder NOS, Sinus arrest... Dose limiting toxicities: Gastrointestinal disorder NOS (50%) Sinus arrest (serious, 16.7%) High grade atrioventricular block (serious, 16.7%) Ventricular escape rhythm (serious, 16.7%) Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj
900 mg single, oral MTD Dose: 900 mg Route: oral Route: single Dose: 900 mg Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	healthy n = 6 Health Status: healthy Population Size: 6 Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj
90 mg 2 times / day multiple, oral Recommended Dose: 90 mg, 2 times / day Route: oral Route: multiple Dose: 90 mg, 2 times / day Co-administed with:: aspirin, p.o Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.3	unhealthy n = 9333 Health Status: unhealthy Condition: acute coronary syndrome Sex: M+F Population Size: 9333 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.3	Disc. AE: Dyspnea... AEs leading to discontinuation/dose reduction: Dyspnea (0.9%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.3
90 mg 2 times / day multiple, oral Recommended Dose: 90 mg, 2 times / day Route: oral Route: multiple Dose: 90 mg, 2 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.1	unhealthy Health Status: unhealthy Condition: acute coronary syndrome Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.1	Disc. AE: Bleeding... AEs leading to discontinuation/dose reduction: Bleeding (grade 3-5) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.1

AEs

AE	Significance	Dose	Population
Gastrointestinal disorder NOS	50% DLT	1260 mg single, oral Highest studied dose Dose: 1260 mg Route: oral Route: single Dose: 1260 mg Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	healthy n = 6 Health Status: healthy Population Size: 6 Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj
High grade atrioventricular block	serious, 16.7% DLT	1260 mg single, oral Highest studied dose Dose: 1260 mg Route: oral Route: single Dose: 1260 mg Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	healthy n = 6 Health Status: healthy Population Size: 6 Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj
Sinus arrest	serious, 16.7% DLT	1260 mg single, oral Highest studied dose Dose: 1260 mg Route: oral Route: single Dose: 1260 mg Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	healthy n = 6 Health Status: healthy Population Size: 6 Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj
Ventricular escape rhythm	serious, 16.7% DLT	1260 mg single, oral Highest studied dose Dose: 1260 mg Route: oral Route: single Dose: 1260 mg Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj	healthy n = 6 Health Status: healthy Population Size: 6 Sources: https://pubmed.ncbi.nlm.nih.gov/24040849 https://www.google.ru/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwji45rs27fuAhVmiYsKHW3hA2MQFjAGegQICBAC&url=https%3A%2F%2Fwww.tga.gov.au%2Ffile%2F797%2Fdownload&usg=AOvVaw3STEHV1bh8A3ZobpKVV1Gj
Dyspnea	0.9% Disc. AE	90 mg 2 times / day multiple, oral Recommended Dose: 90 mg, 2 times / day Route: oral Route: multiple Dose: 90 mg, 2 times / day Co-administed with:: aspirin, p.o Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.3	unhealthy n = 9333 Health Status: unhealthy Condition: acute coronary syndrome Sex: M+F Population Size: 9333 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.3
Bleeding	grade 3-5 Disc. AE	90 mg 2 times / day multiple, oral Recommended Dose: 90 mg, 2 times / day Route: oral Route: multiple Dose: 90 mg, 2 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.1	unhealthy Health Status: unhealthy Condition: acute coronary syndrome Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2016/022433s020lbl.pdf Page: p.1

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
substrate 1737 inhibitor 1587 inducer 781	substrate 1037 inhibitor 1767 inducer 389	substrate 1217 inhibitor 1852	inhibitor 1612

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
Cav1.2 45 Nav1.5 97 Kv1.5 26 Cav3.2 12 CYP3A5 73 CYP1A2 1524 CYP2B6 810 CYP2C8 911 CYP2C19 1478 CYP2E1 882 P-gp 1461 OAT3 642 OAT1 599 UGT1A1 204 L-type Ca channels 9	CYP3A5 395 CYP1A2 1054 CYP2A6 543 CYP2B6 664 CYP2C19 991 P-gp 1537	CYP1A1 108 CYP1A2 701 CYP2B6 547

Drug as perpetrator

Target	Modality	Activity	Metabolite	Clinical evidence
CYP2B6 1001	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=13 Page: 13.0	likely
CYP2B6 1001	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=13 Page: 13.0	likely	AR-C124910XX 3
CYP2C9 1819	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=12 Page: 12-13	likely
CYP2C9 1819	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=12 Page: 12-13	likely	AR-C124910XX 3
CYP2C9 1819	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	moderate [IC50 10.5 uM]
CYP2C19 1553	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	moderate [IC50 11.7 uM]	AR-C124910XX 3
CYP2D6 1891	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	moderate [IC50 26.7 uM]
CYP2B6 1001	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=127 Page: 9-11, (PMDA) 127	moderate [IC50 33 uM]	AR-C124910XX 3
CYP2C8 965	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=127 Page: 9-11, (PMDA) 127	moderate [IC50 43 uM]	AR-C124910XX 3
CYP2C9 1819	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	moderate [IC50 6.9 uM]	AR-C124910XX 3	no (co-administration study) Comment: Human liver microsomes, dicrofenac (substrate); Co-administration of ticagrelor (180 mg BID x 9 days) did not alter the systemic exposure of tolbutamide (500 mg QD on Day 5, CYP2C9 substrate) (GM ratio of AUCinf and Cmax were 103%, 110%, while 4-OH tolbutamide AUCinf GM ratio and Cmax GM ratio were 94% and 90%). Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11
CYP3A5 130	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=130 Page: 9-12, (PMDA) 130	moderate [IC50 7.6 uM]	AR-C124910XX 3
CYP3A5 130	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=60, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=66, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=130 Page: 9-12, 60-61, 66-67, (PMDA) 130	moderate [IC50 8.2 uM]		yes (co-administration study) Comment: Human liver microsomes, midazolam (4-hydroxylation, substrate), no time-dependent inhibition; Co-administration of ticagrelor (270 mg AM + 180 mg PM on Day1, 180 mg BID on Days 2-7) significantly increased simvastatin (80 mg on Day 5, CYP3A4/5 substrate) AUCinf by 56% and Cmax 81%, and simvastatin acid AUCinf by 52% and Cmax by 64%. Co-administration of ticagrelor (270 mg AM + 180 mg PM on Day1, 180 mg BID on Days 2-7) significantly reduced oral midazolam (7.5 mg AM on Days 1 & 7) AUCinf by 10%, and 4’-OH-midazolam by 42%. Co-administration of ticagrelor (270 mg AM + 180 mg PM on Day 1, 180 mg BID on Days 2-7) does not alter the systemic exposure of IV midazolam (2.5 mg IV over 2 min AM on Days 1 & 7) and significantly reduced 4’-OH- midazolam systemic exposure by ~ 23%. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=60, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=66, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=130 Page: 9-12, 60-61, 66-67, (PMDA) 130
CYP2B6 1001	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=127 Page: 9-12, (PMDA) 127	no [IC50 40 uM]
CYP1A2 1692	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	no [IC50 >50 uM]
CYP1A2 1692	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	no [IC50 >50 uM]	AR-C124910XX 3
CYP2C19 1553	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	no [IC50 >50 uM]
CYP2C8 965	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=127 Page: 9-11, (PMDA) 127	no [IC50 >50 uM]
CYP2D6 1891	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	no [IC50 >50 uM]	AR-C124910XX 3
CYP2E1 970	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, Page: 9-11	no [IC50 >50 uM]
CYP3A4 1925	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=62, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=64, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=66, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=124, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=130 Page: 9-12, 62-63, 64-65, 66-67 (PMDA) 124-125, 130	no [IC50 >50 uM]		weak (co-administration study) Comment: Human liver microsomes, midazolam (1-hydroxylation, substrate), midazolam 1-hydroxylation was activated in the presence of Cyt-b5 by 144.9% (CYP3A4 (cDNA expressed enzyme):Cyp-b5 = 1: 3 + 5.56 mcM ticagrelor), no time-dependent inhibition; Inhibited testosterone intrinsic clearance (IC50 = 23 mcM, pooled human liver microsomes (33 male and female donors); Co-administration of ticagrelor (270 mg AM + 90 mg PM on Day 1, 90 mg BID on Days 2-7) significantly increased atorvastatin (80 mg QD on Day 5) AUCinf 36% and Cmax 23%, atorvastatin lactone AUCinf 32% and Cmax 39%, s 2-OH atorvastatin AUCinf 33% and Cmax 13%, and 4-OH atorvastatin AUCinf 67% and Cmax 55%. Co-administration of ticagrelor (90 mg BID x 21 days) significantly increased ethinyl estradiol AUCinf, Cmax, and Cmin by 20%, 30.6%, and 20.2%, respectively. Co-administration of ticagrelor does not alter the systemic exposure of levonorgestrel. Co-administration of ticagrelor (270 mg AM + 180 mg PM on Day1, 180 mg BID on Days 2-7) significantly reduced oral midazolam (7.5 mg AM on Days 1 & 7) AUCinf by 10%, but did not alter 1’-OH- midazolam AUC. Co-administration of ticagrelor (270 mg AM + 180 mg PM on Day 1, 180 mg BID on Days 2-7) did not alter the systemic exposure of IV midazolam (2.5 mg IV over 2 min AM on Days 1 & 7) and 1’-OH-midazolam. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=62, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=64, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=66, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=124, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=130 Page: 9-12, 62-63, 64-65, 66-67 (PMDA) 124-125, 130
CYP1A1 218	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=14, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=139 Page: 14, (PMDA) 139	no
CYP1A2 1692	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=12 Page: 12-13	no
CYP1A2 1692	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=12 Page: 12-13	no	AR-C124910XX 3
CYP3A4 1925	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=12 Page: 12-13	no
CYP3A4 1925	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=12 Page: 12-13	no	AR-C124910XX 3
CYP3A4 1925	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=9, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=130 Page: 9-12, (PMDA) 130	no	AR-C124910XX 3
OAT1 603	inhibitor 3277 Sources: https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=160 Page: (PMDA) 160-161	no
OAT1 603	inhibitor 3277 Sources: https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=160 Page: (PMDA) 160-161	no	AR-C133913XX 3
OAT3 644	inhibitor 3277 Sources: https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=160 Page: (PMDA) 160-161	strong [Ki 13.4 uM]	AR-C133913XX 3
OAT3 644	inhibitor 3277 Sources: https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=160 Page: (PMDA) 160-161	strong [Ki 16.3 uM]	AR-C124910XX 3
OAT3 644	inhibitor 3277 Sources: https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=160 Page: (PMDA) 160-161	strong [Ki 4.9 uM]
OAT1 603	inhibitor 3277 Sources: https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=160 Page: (PMDA) 160-161	strong	AR-C124910XX 3
L-type Ca channels 9	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=116 Page: 116.0	weak
L-type Ca channels 9	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=116 Page: 116.0	weak	AR-C124910XX 3
UGT1A1 254	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 26, 117	yes [IC50 0.759 uM]	AR-C124910XX 3
UGT1A1 254	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 26, 117	yes [IC50 1 uM]
Kv1.5 41	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0	yes [IC50 10 uM]
Kv1.5 41	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0	yes [IC50 16.9 uM]	AR-C124910XX 3
Cav3.2 12	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0	yes [IC50 19.2 uM]
Cav3.2 12	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0	yes [IC50 19.9 uM]	AR-C124910XX 3
P-gp 1650	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=4, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=58, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=157 Page: 4-5, 58-59 (PMDA) 157	yes [IC50 7.8 uM]		yes (co-administration study) Comment: MDR1-MDCK monolayer, H3-digoxin (5 mcM) as a substrate, Flux ratio = 19.5 (digoxin only), 3.1 (digoxin + 10 mcM Ticagrelor); Co-administration of ticagrelor (400 mg QD, Days 1-16) significantly increased digoxin (0.25 mg BID on Day 6, 0.25 mg QD on Days 7-14, P-gp substrate) AUC0-72, Css,max, and Css, min by 28%, 75% and 31%, respectively. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=4, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=58, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=157 Page: 4-5, 58-59 (PMDA) 157
P-gp 1650	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=4, https://www.pmda.go.jp/drugs/2016/P20161026001/670227000_22800AMX00680_I100_1.pdf#page=157 Page: 4-5, (PMDA) 157	yes [IC50 9.9 uM]	AR-C124910XX 3

Drug as victim

Target	Modality	Activity	Metabolite	Clinical evidence
CYP3A4 1737	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=123, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=43 Page: 123, (ClinPharm) 5-6, 43-44, 45-47, 47-49	major [Km 11 uM]		yes (co-administration study) Comment: Human liver microsomes (determination of CYPs) and human cDNA expressed emzymes (Km for AR-C124910XX formation), Km (AR-C124910XX, human liver microsomes) = 27 mcM; Km (AR-C133913XX formation) = 41 mcM; Co-administration of ketoconazole (200 mg BID for 10 days, CYP3A4 inhibitor) significantly increased ticagrelor (90 mg QD on Day 4) AUCinf by 7.32 fold and Cmax by 2.35 fold, and decreased AR-C124910XX AUCinf by 56% and Cmax by 89%. Co-administration of diltiazem (240 mg QD x 14 days, moderate CYP3A4 inhibitor) significantly increased ticagrelor (90 mg QD on Day 8) AUCinf by 2.74 fold and Cmax by 1.69, and decreased AR-C124910XX AUCinf by 13% and Cmax by 38%. Co-administration of rifampin (600 mg QD Days 4-17, strong CYP3A4/P-gp inducer) significantly decreased ticagrelor (180 mg QD Days 1 & 15) AUCinf by 86% and Cmax by 73%, and decreased AR-C124910XX AUCinf by 46% and did not affect Cmax. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=123, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=43 Page: 123, (ClinPharm) 5-6, 43-44, 45-47, 47-49
CYP1A2 1054	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2A6 543	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2B6 664	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C19 991	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C9 1037	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2D6 1217	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP3A5 395	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=123, https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=6 Page: 123, (ClinPharm) 5-6	yes [Km 5.36 uM]
P-gp 1537	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=4 Page: 4.0	yes
P-gp 1537	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000ClinPharmR.pdf#page=4 Page: 4.0	yes	AR-C124910XX 3

Tox targets

Target	Modality	Metabolite
Cav1.2 49	inhibitor 1626 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0
Cav1.2 49	inhibitor 1626 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0	AR-C124910XX 3
Nav1.5 100	inhibitor 1626 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0
Nav1.5 100	inhibitor 1626 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=117 Page: 117.0	AR-C124910XX 3
hERG 1647	inhibitor 1626 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/022433Orig1s000PharmR.pdf#page=119 Page: 119.0

Sourcing

Vendor/Aggregator	ID	URL
ChEBI	CHEBI:68558	https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:68558
ChemicalBook	CB51509134	https://www.chemicalbook.com/ChemicalProductProperty_EN_CB51509134
MolPort	MolPort-023-329-971	https://www.molport.com/shop/molecule-link/MolPort-023-329-971
Selleck Chemicals	ticagrelor	http://www.selleckchem.com/products/ticagrelor.html
ZINC	ZINC000028957444	http://zinc15.docking.org/substances/ZINC000028957444
eMolecules	36756307	https://www.emolecules.com/cgi-bin/more?vid=36756307

PubMed

Title	Date	PubMed
Update on antiplatelet therapy in acute coronary syndromes: what do new drugs bring into clinical practice?	2009	20000883
Test before you stop.	2009 Aug	19687387
[Anticoagulants of primary haemostasis].	2009 Aug	19644598
Ticagrelor yields consistent dose-dependent inhibition of ADP-induced platelet aggregation in patients with atherosclerotic disease regardless of genotypic variations in P2RY12, P2RY1, and ITGB3.	2009 Aug	19637098
P2Y(12) inhibitors: differences in properties and mechanisms of action and potential consequences for clinical use.	2009 Aug	19633016
Ticagrelor--a new platelet aggregation inhibitor in patients with acute coronary syndromes. An improvement of other inhibitors?	2009 Dec	19946242
Antiplatelet therapy: Ticagrelor in ACS-what does PLATO teach us?	2009 Dec	19935680
Oral antiplatelet therapy for acute and chronic management of NSTE ACS: residual ischemic risk and opportunities for improvement.	2009 Dec	19890703
Ticagrelor versus clopidogrel in acute coronary syndromes.	2009 Dec 10	20050198
Ticagrelor versus clopidogrel in acute coronary syndromes.	2009 Dec 10	20050197
Ticagrelor versus clopidogrel in acute coronary syndromes.	2009 Dec 10	20007565
ACP Journal Club. Ticagrelor was more effective than clopidogrel, with no increase in major bleeding in acute coronary syndromes.	2009 Dec 15	20008753
Randomized double-blind assessment of the ONSET and OFFSET of the antiplatelet effects of ticagrelor versus clopidogrel in patients with stable coronary artery disease: the ONSET/OFFSET study.	2009 Dec 22	19923168
New P2Y12 blockers.	2009 Jul	19630813
Future of oral antiplatelet therapy: four challenged hypotheses.	2009 Jun	19492145
Update on oral antiplatelet therapy: principles, problems and promises.	2009 May	19450051
Strategy for the treatment of clopidogrel low responsiveness in diabetes mellitus and stent implantation.	2009 Nov	19997540
HOTLINE I, PLATO favours ticagrelor over clopidogrel in ACS.	2009 Nov	19891080
P2Y12 inhibitors: thienopyridines and direct oral inhibitors.	2009 Nov	19882081
European Society of Cardiology--2009 annual congress. 31 August - 2 September 2009, Barcelona, Spain.	2009 Nov	19844849
Comparison of ticagrelor and thienopyridine P2Y(12) binding characteristics and antithrombotic and bleeding effects in rat and dog models of thrombosis/hemostasis.	2009 Nov	19692114
Ticagrelor binds to human P2Y(12) independently from ADP but antagonizes ADP-induced receptor signaling and platelet aggregation.	2009 Sep	19552634
New P2Y12 antagonists.	2009 Sep	19550317
Ticagrelor versus clopidogrel in patients with acute coronary syndromes.	2009 Sep 10	19717846
Ticagrelor--is there need for a new player in the antiplatelet-therapy field?	2009 Sep 10	19717845
Ticagrelor: the first reversibly binding oral P2Y12 receptor antagonist.	2009 Winter	19604248
[Ticagrelor versus clopidogrel in patients with acute coronary syndromes: results of the PLATO study].	2010	20144161
Antiplatelet therapy prasugrel: a novel platelet ADP P2Y12 receptor antagonist.	2010 Apr	20299391
The PLATO trial: do you believe in magic?	2010 Apr	20007979
Balancing the benefits and risks of antiplatelet agents in patients with non-ST-segment elevated acute coronary syndromes and undergoing percutaneous coronary intervention.	2010 Aug	20111983
Mechanism of action and clinical development of ticagrelor, a novel platelet ADP P2Y12 receptor antagonist.	2010 Feb	20136601
The year in cardiothoracic and vascular anesthesia: selected highlights from 2009.	2010 Feb	20123237
Limitations of current therapies to prevent thrombosis: a need for novel strategies.	2010 Feb	20094648
New drugs for the treatment of coronary artery syndromes: otamixaban and ticagrelor.	2010 Feb	20088750
Pharmacokinetic, pharmacodynamic and clinical profile of novel antiplatelet drugs targeting vascular diseases.	2010 Feb 1	20050853
Emerging P2Y12 receptor antagonists: role in coronary artery disease.	2010 Jan	19485932
[Update on new antithrombotic treatments].	2010 Jan 20	20170027
Ticagrelor in ACS: redefining a new standard of care?	2010 Jan 23	20079529
Comparison of ticagrelor with clopidogrel in patients with a planned invasive strategy for acute coronary syndromes (PLATO): a randomised double-blind study.	2010 Jan 23	20079528
The case for routine genotyping in dual-antiplatelet therapy.	2010 Jul 6	20471193
Advances in antiplatelet therapy for stroke prevention: the new P2Y12 antagonists.	2010 Mar	20210760
Efficacy and safety of ticagrelor: a reversible P2Y12 receptor antagonist.	2010 Mar	20124464
The novel P2Y 12 antagonist AZD6140 rapidly and reversibly reduces platelet activation in diabetic rats.	2010 Mar	19846210
Role of ticagrelor in clopidogrel nonresponders: resistance is futile?	2010 Mar 16	20194888
Response to ticagrelor in clopidogrel nonresponders and responders and effect of switching therapies: the RESPOND study.	2010 Mar 16	20194878
Pharmacokinetics, pharmacodynamics, tolerability and safety of single ascending doses of ticagrelor, a reversibly binding oral P2Y(12) receptor antagonist, in healthy subjects.	2010 May	20091161
Advances in antiplatelet treatment for acute coronary syndromes.	2010 May	19910292
Forecasting drug utilization and expenditure in a metropolitan health region.	2010 May 17	20478043
The year in interventional cardiology.	2010 May 18	20466207
State of the art of new P2Y12 antagonists.	2010 Oct	20177818

Patents

Sample Use Guides

In Vivo Use Guide

Initiate treatment with 180 mg (two 90 mg tablets) oral loading dose. Continue treatment with 90 mg twice daily.

Route of Administration: Oral

In Vitro Use Guide

In human liver microsomes, ticagrelor inhibited midazolam 4-hydroxylation with an IC50 of 8.2 uM. Evaluated in fresh human hepatocytes at concentration up to 20 uM, ticagrelor was not an inducer of CYP1A2 or CYP3A4.

Substance Class	Chemical Created by `admin` on `Fri Dec 15 16:04:36 GMT 2023` Edited by `admin` on `Fri Dec 15 16:04:36 GMT 2023`
Record UNII	GLH0314RVC
Record Status	`Validated (UNII)`
Record Version

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Name

Type

Language

TICAGRELOR

Official Name

English

BRILINTA

Brand Name

English

1,2-CYCLOPENTANEDIOL, 3-(7-(((1R,2S)-2-(3,4-DIFLUOROPHENYL)CYCLOPROPYL)AMINO)-5-(PROPYLTHIO)-3H-1,2,3-TRIAZOLO(4,5-D)PYRIMIDIN-3-YL)-5-(2-HYDROXYETHOXY)-, (1S,2S,3R,5S)-

Systematic Name

English

AZD-6140

Code

English

TICAGRELOR [MI]

Common Name

English

(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

Systematic Name

English

POSSIA

Brand Name

English

TICAGRELOR [EMA EPAR]

Common Name

English

Ticagrelor [WHO-DD]

Common Name

English

TICAGRELOR [EP MONOGRAPH]

Common Name

English

TICAGRELOR [USAN]

Common Name

English

TICAGRELOR [ORANGE BOOK]

Common Name

English

ticagrelor [INN]

Common Name

English

TICAGRELOR [USP-RS]

Common Name

English

TICAGRELOR [JAN]

Common Name

English

TICAGRELOR [MART.]

Common Name

English

AZD6140

Code

English

BRILIQUE

Brand Name

English

AR-C126532XX

Code

English

TICAGRELOR [VANDF]

Common Name

English

Classification Tree Code System Code

EMA ASSESSMENT REPORTS

POSSIA (WITHDRAWN: PERIPHERAL VASCULAR DISEASES)