BMS-817399

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Search structure


Synonyms	Bms-817399
Status
Molecule Category	UNKNOWN
UNII	AKQ3X6FEH0


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

Structure


InChI Key	GTDPZONCGOCXOD-JPYJTQIMSA-N
Smiles	CC(C)[C@@H](NC(=O)NCC(C)(C)O)C(=O)N1CC[C@](O)(c2ccc(Cl)cc2)C(C)(C)C1
InChI	InChI=1S/C23H36ClN3O4/c1-15(2)18(26-20(29)25-13-22(5,6)30)19(28)27-12-11-23(31,21(3,4)14-27)16-7-9-17(24)10-8-16/h7-10,15,18,30-31H,11-14H2,1-6H3,(H2,25,26,29)/t18-,23+/m1/s1

Physicochemical Descriptors

Property Name	Value
Molecular Formula	C23H36ClN3O4
Molecular Weight	454.01
AlogP	2.88
Hydrogen Bond Acceptor	4.0
Hydrogen Bond Donor	4.0
Number of Rotational Bond	6.0
Polar Surface Area	101.9
Molecular species	NEUTRAL
Aromatic Rings	1.0
Heavy Atoms	31.0

Bioactivity

Mechanism of Action	Action	Reference
C-C chemokine receptor type 1 antagonist	ANTAGONIST	PubMed Other


Protein: C-C chemokine receptor type 1 Description: C-C chemokine receptor type 1 Organism : Homo sapiens P32246 ENSG00000163823

Targets	EC50(nM)	IC50(nM)	Kd(nM)	Ki(nM)	Inhibition(%)
Membrane receptor Family A G protein-coupled receptor Peptide receptor (family A GPCR) Chemokine receptor CC chemokine receptor	-	1-42	-	-	-

Assay Description	Organism	Bioactivity	Reference
Displacement of [125I]MIP-1alpha from CCR1 in human THP1 cells	Homo sapiens	1.0 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of MIP-1alpha induced chemotaxis after 60 mins	Homo sapiens	6.0 nM
Displacement of [125I]hMIP-1alpha from CCR1 in human PBMC	Homo sapiens	4.2 nM
Displacement of [125I]hMIP-1alpha from dog PBMC CCR1	Canis lupus familiaris	635.0 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of MIP-1alpha-induced chemotaxis after 60 mins	Homo sapiens	5.5 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of RANTES-induced chemotaxis after 60 mins	Homo sapiens	3.3 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of MCP3-induced chemotaxis after 60 mins	Homo sapiens	9.3 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of HCC1-induced chemotaxis after 60 mins	Homo sapiens	7.5 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of LKN1-induced chemotaxis after 60 mins	Homo sapiens	16.2 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of HCC4-induced chemotaxis after 60 mins	Homo sapiens	3.2 nM
Antagonist activity at CCR1 receptor in human THP1 cells assessed as inhibition of MPIF1-induced chemotaxis after 60 mins	Homo sapiens	14.3 nM
Antagonist activity at CCR1 receptor in human whole blood assessed as blocked of MIP-1alpha-mediated CD11b upregulation preincubated for 1 hr	Homo sapiens	25.0 nM
Antagonist activity at CCR1 receptor in human whole blood assessed as blocked of LKN1-mediated CD11b upregulation preincubated for 1 hr	Homo sapiens	42.0 nM
Antagonist activity at recombinant CCR1 (unknown origin) expressed in non-adherent cells co-expressing Galpha16 assessed as inhibition of MIP-1 alpha-induced calcium flux by Fluo-4 NW or Calcium 4 dye based FLIPR TETRA assay	Homo sapiens	3.0 nM
Antagonist activity at CCR1 in human THP1 cells assessed as inhibition of chemotaxis after 30 mins by Celltiter-glo reagent based luminescence assay	Homo sapiens	1.5 nM

Cross References

Resources	Reference
ChEMBL	CHEMBL3334824
DrugBank	DB14941
FDA SRS	AKQ3X6FEH0
Guide to Pharmacology	9497
PubChem	44537841
SureChEMBL	SCHEMBL1604247

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).