SELEXIPAG

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Search structure


Trade Names	UPTRAVI
Synonyms	ACT-293987 NS-304 Selexipag Uptravi
Status
Molecule Category	UNKNOWN
ATC	B01AC27
UNII	5EXC0E384L


Active Pharmaceutical Ingredients Bioactive chemicals	Exact Similarity SubStructure	Threshold (%) >= 70

Structure


InChI Key	QXWZQTURMXZVHJ-UHFFFAOYSA-N
Smiles	CC(C)N(CCCCOCC(=O)NS(C)(=O)=O)c1cnc(-c2ccccc2)c(-c2ccccc2)n1
InChI	InChI=1S/C26H32N4O4S/c1-20(2)30(16-10-11-17-34-19-24(31)29-35(3,32)33)23-18-27-25(21-12-6-4-7-13-21)26(28-23)22-14-8-5-9-15-22/h4-9,12-15,18,20H,10-11,16-17,19H2,1-3H3,(H,29,31)

Physicochemical Descriptors

Property Name	Value
Molecular Formula	C26H32N4O4S
Molecular Weight	496.63
AlogP	3.9
Hydrogen Bond Acceptor	7.0
Hydrogen Bond Donor	1.0
Number of Rotational Bond	12.0
Polar Surface Area	101.49
Molecular species	ACID
Aromatic Rings	3.0
Heavy Atoms	35.0

Bioactivity

Mechanism of Action	Action	Reference
Prostanoid IP receptor agonist	AGONIST	FDA


Protein: Prostanoid IP receptor Description: Prostacyclin receptor Organism : Homo sapiens P43119 ENSG00000160013

Targets	EC50(nM)	IC50(nM)	Kd(nM)	Ki(nM)	Inhibition(%)
Membrane receptor Family A G protein-coupled receptor Small molecule receptor (family A GPCR) Lipid-like ligand receptor (family A GPCR) Prostanoid receptor	100	62	-	-	-

Assay Description	Organism	Bioactivity	Reference
Agonist activity at recombinant rat IP receptor expressed in CHO-K1 cells assessed as increase in intracellular cAMP level after 1 hr incubation by HTRF method	Rattus norvegicus	200.0 nM
Agonist activity at recombinant human IP receptor expressed in CHO-K1 cells assessed as increase in intracellular cAMP level after 1 hr incubation by HTRF method	Homo sapiens	6.0 nM
Agonist activity at recombinant human DP1 receptor expressed in CHO-K1 cells assessed as increase in intracellular cAMP level after 1 hr incubation by HTRF method	Homo sapiens	100.0 nM
Agonist activity at IP receptor in human primary platelets assessed as inhibition of ADP-induced platelet aggregation	Homo sapiens	62.0 nM
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells at 10 uM after 48 hours by high content imaging	Homo sapiens	-2.21 %
SARS-CoV-2 3CL-Pro protease inhibition percentage at 20µM by FRET kind of response from peptide substrate	Severe acute respiratory syndrome coronavirus 2	15.4 %		SARS-CoV-2 3CL-Pro protease inhibition percentage at 20µM by FRET kind of response from peptide substrate	Severe acute respiratory syndrome coronavirus 2	10.87 %
Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging	Chlorocebus sabaeus	0.35 %		Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging	Chlorocebus sabaeus	-0.08 %		Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging	Chlorocebus sabaeus	0.35 %		Antiviral activity determined as inhibition of SARS-CoV-2 induced cytotoxicity of VERO-6 cells at 10 uM after 48 hours exposure to 0.01 MOI SARS CoV-2 virus by high content imaging	Chlorocebus sabaeus	-0.08 %

Cross References

Resources	Reference
ChEBI	90844
ChEMBL	CHEMBL238804
DrugBank	DB11362
DrugCentral	5077
FDA SRS	5EXC0E384L
Guide to Pharmacology	7552
PubChem	9913767
SureChEMBL	SCHEMBL674122
ZINC	ZINC000003990451

CONTENTS

PREMIER has received funding from the Innovative Medicines Initiative 2 Joint Undertaking (JU) under grant agreement No 875508. The JU receives support from the EU’s Horizon 2020 research and innovation programme and the European Federation of Pharmaceutical Industries and Associations (EFPIA). The views reflect only the authors’ perspective and the JU is not responsible for any use that may be made of the information this manuscript contains.

Elements of the website have been developed under projects PREMIER and the Biocenter Finland Drug Discovery and Chemical Biology network. CSC-IT is thanked for providing computational resources. Content of the website is provided without guarantee for correctness. Data has been collected and integrated from multiple public sources, for the largest: FDA, HUGO Gene Nomenclature Committee, ChEMBL, IUPHAR/BPS guide to pharmacology, Reactome, UniProt, and Ensembl. Credit is given to Ensembl for collecting species images (provided under public domain licences such as Wikimedia and NHGRI).