PALMIDROL

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Search structure


Synonyms	AM 3112 FSD-201 Impulsin Levagen Loramine p 256 N(2-hydroxyethyl) palmitide N(2-hydroxyethyl)palmitide N-(2-hydroxyethyl)-palmitide NSC-23320 Palmdrol prodes Palmidrol Palmitamide mea Palmitic acid monoethanolamide Palmitic monoethanolamide Palmitoyl ethanolamide Palmitoylethanolamide
Status
Molecule Category	UNKNOWN
UNII	6R8T1UDM3V
EPA CompTox	DTXSID4042254


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

Structure


InChI Key	HXYVTAGFYLMHSO-UHFFFAOYSA-N
Smiles	CCCCCCCCCCCCCCCC(=O)NCCO
InChI	InChI=1S/C18H37NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-18(21)19-16-17-20/h20H,2-17H2,1H3,(H,19,21)

Physicochemical Descriptors

Property Name	Value
Molecular Formula	C18H37NO2
Molecular Weight	299.5
AlogP	4.58
Hydrogen Bond Acceptor	2.0
Hydrogen Bond Donor	2.0
Number of Rotational Bond	16.0
Polar Surface Area	49.33
Molecular species	NEUTRAL
Aromatic Rings	0.0
Heavy Atoms	21.0

Assay Description	Organism	Bioactivity	Reference
Binding affinity against human Cannabinoid receptor 1 using CHO-hCB1 transfected cell membrane and [3H]CP-55940 as radioligand at 10 uM	None	24.0 %
Percent inhibition of specific binding of [3H]CP-55940 towards human cannabinoid receptor 1 from Chinese hamster ovary cell membranes at the concentration of 10 uM	None	23.8 %
% inhibition of specific binding of [3H]Win55,212-2 towards human Cannabinoid receptor 2 from Chinese hamster ovary cell membranes at 10 uM	None	13.9 %
Binding affinity against human CB2 receptor by using CHO-hCB2 transfected cell membrane [3H]WIN-55212-2 as radioligand at 10 uM	None	14.0 %
Inhibition of fatty acid amide hydrolase (FAAH) from rat brain homogenates at 10 uM	None	49.0 %
Inhibition of fatty acid amide hydrolase (FAAH) from rat brain homogenates at 100 uM	None	68.0 %
Inhibition of N-palmitoylethanolamine-selective acid amidase (NPAA) from rat lung homogenates at 100 uM	None	34.0 %
Inhibition of AEA (N-arachidonoylethanolamine) metabolism using rat brain homogenates at pH 6 using [3H]-anandamide as the labeled substrate	Rattus norvegicus	62.0 %
Inhibition of AEA (N-arachidonoylethanolamine) metabolism using rat brain homogenates at pH 9 using [3H]anandamide as the labeled substrate	Rattus norvegicus	100.0 %
Percent inhibition of AEA (N-arachidonoylethanolamine) metabolism in rat brain homogenates using [3H]anandamide as the labeled substrate.	Rattus norvegicus	78.0 %
Antiplasmodial activity against Plasmodium falciparum GB4 after 72 hrs by SYBR green assay	Plasmodium falciparum	501.19 nM
Antidepressant activity in Mus musculus Kunming (mouse) assessed as reduction in duration of immobility at 10 mg/kg, ip measured after 30 min by forced swim test	Mus musculus	6.25 %
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	-3.5 %
Inhibition of ARAT in bovine RPE microsomes at 10 uM using retinol substrate in presence of dilauroyl-phosphatidyl choline incubated for 5 mins by HPLC analysis relative to control	Bos taurus	6.0 %
Inhibition of ARAT in bovine RPE microsomes at 100 uM using retinol substrate in presence of dilauroyl-phosphatidyl choline incubated for 5 mins by HPLC analysis relative to control	Bos taurus	23.0 %
Inhibition of LRAT in bovine RPE microsomes at 10 uM using retinol substrate in presence of Palmitoyl-CoA incubated for 5 mins by HPLC analysis relative to control	Bos taurus	12.0 %
Inhibition of LRAT in bovine RPE microsomes at 100 uM using retinol substrate in presence of Palmitoyl-CoA incubated for 5 mins by HPLC analysis relative to control	Bos taurus	33.0 %
SARS-CoV-2 3CL-Pro protease inhibition percentage at 20µM by FRET kind of response from peptide substrate	Severe acute respiratory syndrome coronavirus 2	24.17 %		SARS-CoV-2 3CL-Pro protease inhibition percentage at 20µM by FRET kind of response from peptide substrate	Severe acute respiratory syndrome coronavirus 2	20.53 %		SARS-CoV-2 3CL-Pro protease inhibition percentage at 20µM by FRET kind of response from peptide substrate	Severe acute respiratory syndrome coronavirus 2	3.157 %
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	-0.19 %		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	0.03 %		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	0.03 %		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	-0.19 %

Related Entries

Cross References

Resources	Reference
ChEBI	71464
ChEMBL	CHEMBL417675
DrugBank	DB14043
DrugCentral	2045
FDA SRS	6R8T1UDM3V
Human Metabolome Database	HMDB0002100
Guide to Pharmacology	3622
KEGG	C16512
PubChem	4671
SureChEMBL	SCHEMBL19511663
ZINC	ZINC000008035017

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).