FENFLURAMINE HYDROCHLORIDE

First approved in 1973

Details

Stereochemistry	RACEMIC
Molecular Formula	C12H16F3N.ClH
Molecular Weight	267.718
Optical Activity	( + / - )
Defined Stereocenters	0 / 1
E/Z Centers	0
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

Cl.CCNC(C)CC1=CC(=CC=C1)C(F)(F)F

InChI

InChIKey=ZXKXJHAOUFHNAS-UHFFFAOYSA-N

InChI=1S/C12H16F3N.ClH/c1-3-16-9(2)7-10-5-4-6-11(8-10)12(13,14)15;/h4-6,8-9,16H,3,7H2,1-2H3;1H

HIDE SMILES / InChI

Molecular Formula	ClH
Molecular Weight	36.461
Charge	0
Count

Stereochemistry	ACHIRAL
Additional Stereochemistry	No
Defined Stereocenters	0 / 0
E/Z Centers	0
Optical Activity	NONE

Molecular Formula	C12H16F3N
Molecular Weight	231.2573
Charge	0
Count

Stereochemistry	RACEMIC
Additional Stereochemistry	No
Defined Stereocenters	0 / 1
E/Z Centers	0
Optical Activity	( + / - )

Description
Sources: https://www.drugbank.ca/drugs/DB00574
Curator's Comment: description was created based on several sources, including https://www.drugs.com/international/fenfluramine.html | https://www.ncbi.nlm.nih.gov/pubmed/24790728 | https://clinicaltrials.gov/ct2/show/NCT02655198 | https://www.ncbi.nlm.nih.gov/pubmed/27264138 | https://www.ncbi.nlm.nih.gov/pubmed/22554283 | https://www.ncbi.nlm.nih.gov/pubmed/26600876

Fenfluramine (former brand names Pondimin, Ponderax and Adifax), also known as 3-trifluoromethyl-N-ethylamphetamine, is an anorectic that is no longer marketed. In combination with phentermine, it was part of the anti-obesity medication Fen-phen. Fenfluramine was introduced on the U.S. market in 1973 and withdrawn in 1997. It is the racemic mixture of two enantiomers, dexfenfluramine, and levofenfluramine. The drug increases the level of serotonin, a neurotransmitter that regulates mood, appetite and other functions. Fenfluramine causes the release of serotonin by disrupting vesicular storage of the neurotransmitter and reversing serotonin transporter function. The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease and pulmonary hypertension, including a condition known as cardiac fibrosis. It was subsequently withdrawn from other markets around the world. In this small exploratory and retrospective study, remarkably good results were reported on the use of fenfluramine as an add-on medication for controlling seizures in patients with the Dravet syndrome. The side effects were rare and nonserious and did not result in termination of the treatment. It is possible that this drug may have anticonvulsive effects for other severe epilepsy syndromes, especially in those characterized by photosensitive or induced seizures.

CNS Activity

Originator

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
serotonin secretion 8 Target ID: GO:0001820 Sources: https://www.ncbi.nlm.nih.gov/pubmed/16237679	Activator 1447

Conditions

Condition	Modality	Highest Phase	Product
Obesity 206 Sources: http://www.rxlist.com/pondimin-drug/indications-dosage.htm	Primary	Approved 8583	Pondimin Approved Use Unknown
Epilepsy 121 Sources: https://clinicaltrials.gov/ct2/show/NCT02655198	Primary	Phase II 1147	Pondimin Approved Use Unknown
Lennox gastaut syndrome 2 Sources: https://clinicaltrials.gov/ct2/show/NCT02655198	Primary	Phase II 1147	Pondimin Approved Use Unknown
Dravet syndrome 5 Sources: https://clinicaltrials.gov/ct2/show/NCT02682927	Primary	Phase III 665	Pondimin Approved Use Unknown
Seizure disorders 4 Sources: https://clinicaltrials.gov/ct2/show/NCT02682927	Primary	Phase III 665	Pondimin Approved Use Unknown

C_max

Value	Dose	Co-administered	Analyte	Population
68 ng/mL DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf	0.35 mg/kg 2 times / day steady-state, oral dose: 0.35 mg/kg route of administration: Oral experiment type: STEADY-STATE co-administered:		FENFLURAMINE plasma	Homo sapiens population: UNHEALTHY age: CHILD sex: UNKNOWN food status: UNKNOWN

AUC

Value	Dose	Co-administered	Analyte	Population
1390 ng × h/mL DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf	0.35 mg/kg 2 times / day steady-state, oral dose: 0.35 mg/kg route of administration: Oral experiment type: STEADY-STATE co-administered:		FENFLURAMINE plasma	Homo sapiens population: UNHEALTHY age: CHILD sex: UNKNOWN food status: UNKNOWN

T_1/2

Value	Dose	Co-administered	Analyte	Population
20 h DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf	0.35 mg/kg 2 times / day steady-state, oral dose: 0.35 mg/kg route of administration: Oral experiment type: STEADY-STATE co-administered:		FENFLURAMINE plasma	Homo sapiens population: UNHEALTHY age: CHILD sex: UNKNOWN food status: UNKNOWN

F_unbound

Value	Dose	Co-administered	Analyte	Population
50% DRUG LABEL https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf	0.35 mg/kg 2 times / day steady-state, oral dose: 0.35 mg/kg route of administration: Oral experiment type: STEADY-STATE co-administered:		FENFLURAMINE plasma	Homo sapiens population: UNHEALTHY age: CHILD sex: UNKNOWN food status: UNKNOWN

Doses

Dose	Population	Adverse events
60 mg/day 1 times / day steady, oral Highest studied dose Dose: 60 mg/day, 1 times / day Route: oral Route: steady Dose: 60 mg/day, 1 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/3134879/	unhealthy, 11 years Health Status: unhealthy Age Group: 11 years Sex: F Sources: https://pubmed.ncbi.nlm.nih.gov/3134879/	Sources: https://pubmed.ncbi.nlm.nih.gov/3134879/
0.2 mg/kg/day 2 times / day steady, oral Studied dose Dose: 0.2 mg/kg/day, 2 times / day Route: oral Route: steady Dose: 0.2 mg/kg/day, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30146701	unhealthy, 11.7 ± 4.4 years (range: 3‐17 years) Health Status: unhealthy Age Group: 11.7 ± 4.4 years (range: 3‐17 years) Sex: M+F Sources: https://pubmed.ncbi.nlm.nih.gov/30146701	Other AEs: Decreased appetite... Other AEs: Decreased appetite (2 patients) Sources: https://pubmed.ncbi.nlm.nih.gov/30146701
0.7 mg/kg/day 1 times / day steady, oral Studied dose Dose: 0.7 mg/kg/day, 1 times / day Route: oral Route: steady Dose: 0.7 mg/kg/day, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf	unhealthy Health Status: unhealthy Sex: unknown Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf	Disc. AE: Somnolence... AEs leading to discontinuation/dose reduction: Somnolence (3.3%) Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf

AEs

AE	Significance	Dose	Population
Decreased appetite	2 patients	0.2 mg/kg/day 2 times / day steady, oral Studied dose Dose: 0.2 mg/kg/day, 2 times / day Route: oral Route: steady Dose: 0.2 mg/kg/day, 2 times / day Sources: https://pubmed.ncbi.nlm.nih.gov/30146701	unhealthy, 11.7 ± 4.4 years (range: 3‐17 years) Health Status: unhealthy Age Group: 11.7 ± 4.4 years (range: 3‐17 years) Sex: M+F Sources: https://pubmed.ncbi.nlm.nih.gov/30146701
Somnolence	3.3% Disc. AE	0.7 mg/kg/day 1 times / day steady, oral Studied dose Dose: 0.7 mg/kg/day, 1 times / day Route: oral Route: steady Dose: 0.7 mg/kg/day, 1 times / day Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf	unhealthy Health Status: unhealthy Sex: unknown Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
inhibitor 2252 inducer 1087	substrate 1193 inhibitor 2438 inducer 440	substrate 1388 inhibitor 2507 inducer 109

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP1A2 2153 CYP2B6 926 CYP2C8 1057 CYP2C19 2057 P-gp 1741 BCRP 910 OATP1B1 1079 OATP1B3 961 OAT1 725 OAT3 747 OCT2 779 MATE1 415 MATE2 267	CYP1A2 1197 CYP2B6 776 CYP2C19 1119 CYP3A4/5 91 OAT3 391 OCT2 434 MATE1 182 MATE2 98 BCRP 697 OAT1 395	CYP1A2 832 CYP2B6 669 CYP2C8 198 CYP2C19 329

Drug as perpetrator

Target	Modality	Activity	Metabolite
BCRP 985	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 985	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP1A2 2333	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1A2 2333	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1A2 2333	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2B6 1160	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2B6 1160	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2B6 1160	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2C19 2141	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C19 2141	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C19 2141	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2C8 1117	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C8 1117	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C8 1117	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2C9 2497	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C9 2497	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C9 2497	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2D6 2546	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2D6 2546	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2D6 2546	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP3A4 2633	inducer 1966 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP3A4 2633	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP3A4 2633	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE1 416	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE1 416	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE2 267	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE2 267	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT1 730	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT1 730	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT3 749	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT3 749	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OATP1B1 1095	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OATP1B1 1095	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OATP1B3 970	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OATP1B3 970	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OCT2 782	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OCT2 782	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
P-gp 1932	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
P-gp 1932	inhibitor 4027 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2

Drug as victim

Target	Modality	Activity	Metabolite	Clinical evidence
CYP2C9 1193	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	minor
CYP2C19 1119	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	minor		unlikely (co-administration study) Comment: The effect of coadministration of CBD on fenfluramine and norfenfluramine PK was evaluated in Study 1604. The study demonstrated that co-administration of CBD with ZX008 increased fenfluramine AUC0-t by approximately 59% and the Cmax was not changed significantly. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0
CYP3A4/5 91	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	minor		unlikely (co-administration study) Comment: The effect of coadministration of CBD on fenfluramine and norfenfluramine PK was evaluated in Study 1604. The study demonstrated that co-administration of CBD with ZX008 increased fenfluramine AUC0-t by approximately 59% and the Cmax was not changed significantly. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0
BCRP 697	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 697	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE1 182	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE1 182	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE2 98	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE2 98	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT1 395	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT1 395	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT3 391	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT3 391	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OCT2 434	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OCT2 434	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2D6 1388	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP1A2 1197	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes		unlikely (co-administration study) Comment: The effect of coadministration of CBD on fenfluramine and norfenfluramine PK was evaluated in Study 1604. The study demonstrated that co-administration of CBD with ZX008 increased fenfluramine AUC0-t by approximately 59% and the Cmax was not changed significantly. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0
CYP2B6 776	substrate 4014 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes		unlikely (co-administration study) Comment: The effect of coadministration of CBD on fenfluramine and norfenfluramine PK was evaluated in Study 1604. The study demonstrated that co-administration of CBD with ZX008 increased fenfluramine AUC0-t by approximately 59% and the Cmax was not changed significantly. Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0

Tox targets

Target	Modality	Activity	Metabolite	Clinical evidence
Nav1.5 119	binder 5 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000OtherR.pdf#page=38 Page: 38.0

Sourcing

Vendor/Aggregator	ID	URL
ChEBI	CHEBI:59729	https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:59729
eMolecules	538306	https://www.emolecules.com/cgi-bin/more?vid=538306

PubMed

Title	Date	PubMed
Retest reliability of prolactin response to dl-fenfluramine challenge in adults.	2002-02	11790522
Inhibition of cocaine self-administration by fluoxetine or D-fenfluramine combined with phentermine.	2002-01-29	11812523
Is long-term heavy alcohol consumption toxic for brain serotonergic neurons? Relationship between years of excessive alcohol consumption and serotonergic neurotransmission.	2002-01-01	11772477
Pharmacological studies of the acute effects of (+)-3,4-methylenedioxymethamphetamine on locomotor activity: role of 5-HT(1B/1D) and 5-HT(2) receptors.	2002-01	11751031
Anorexigen-induced pulmonary hypertension and the serotonin (5-HT) hypothesis: lessons for the future in pathogenesis.	2002	11806844
Aortic and mitral fenfluramine-phentermine valvulopathy in 64 patients treated with anorectic agents.	2001-12	11735689
LY393558, a 5-hydroxytryptamine reuptake inhibitor and 5-HT(1B/1D) receptor antagonist: effects on extracellular levels of 5-hydroxytryptamine in the guinea pig and rat.	2001-11-30	11734183
MDMA and fenfluramine alter the response of the circadian clock to a serotonin agonist in vitro.	2001-11-30	11716826
Fenfluramine and phentermine.	2001-11-06	11694113
Fluorometric determination of DL-fenfluramine, DL-norfenfluramine and phentermine in plasma by achiral and chiral high-performance liquid chromatography.	2001-11-05	11710586
Clinical and echocardiographic follow-up of patients previously treated with dexfenfluramine or phentermine/fenfluramine.	2001-11-03	11667938
Effects of endogenous neurotransmitters on the in vivo binding of dopamine and 5-HT radiotracers in mice.	2001-11	11682251
Monoamine oxidase inhibition is unlikely to be relevant to the risks associated with phentermine and fenfluramine: a comparison with their abilities to evoke monoamine release.	2001-10	11673765
Operation for anorexigen-associated valvular heart disease.	2001-10	11581595
High performance liquid chromatography with UV detection for the simultaneous determination of sympathomimetic amines using 4-(4,5-diphenyl-1H-imidazole-2-yl)benzoyl chloride as a label.	2001-10	11559922
Neuroendocrine effects of d-fenfluramine and bromocriptine following repeated smoked cocaine in humans.	2001-09-01	11470342
Acute effects of D-fenfluramine on simultaneous measures of aggressive escape and impulsive responses of adult males with and without a history of conduct disorder.	2001-09	11605076
Acute anorectic effect of single and combined drugs in mice using a non-deprivation protocol.	2001-09	11594445
Risk factors for pulmonary arterial hypertension.	2001-09	11590841
The relationship between health-related quality of life and weight loss.	2001-09	11557837
Prolactin response to dl-fenfluramine challenge before and after treatment with paroxetine.	2001-09	11522467
Relationship between central serotonergic neurotransmission and reduction in alcohol intake by citalopram.	2001-08-01	11418230
Neuroendocrine serotonergic and dopaminergic responsivity in male schizophrenic patients during treatment with neuroleptics and after switch to risperidone.	2001-08	11512043
Hypothalamo-pituitary-adrenal axis dysfunction in chronic fatigue syndrome, and the effects of low-dose hydrocortisone therapy.	2001-08	11502777
Effects of dietary sucrose on hippocampal serotonin release: a microdialysis study in the freely-moving rat.	2001-08	11502227
Evidence that hypophagia induced by d-fenfluramine and d-norfenfluramine in the rat is mediated by 5-HT2C receptors.	2001-08	11489456
Fenfluramine-induced pulmonary vasoconstriction: role of serotonin receptors and potassium channels.	2001-08	11457791
Effect of 5-HT on binding of [(11)C] WAY 100635 to 5-HT(IA) receptors in rat brain, assessed using in vivo microdialysis nd PET after fenfluramine.	2001-08	11400181
Pharmacologic options for the treatment of obesity.	2001-07-15	11471477
Low risk of significant echocardiographic valvulopathy in patients treated with anorectic drugs.	2001-07	11461737
Lack of effect of HPA axis hyperactivity on hormonal responses to d-fenfluramine in major depressed patients: implications for pathogenesis of suicidal behaviour.	2001-07	11337135
Prolactin response to d-fenfluramine in postmenopausal women on and off ERT: comparison with young women.	2001-07	11337133
Too late, again?	2001-06-23	11420587
[Serotonin receptor changes in depression: evidences and limitations].	2001-06-20	11412493
Echocardiographic examination of women previously treated with fenfluramine: long-term follow-up of a randomized, double-blind, placebo-controlled trial.	2001-06-11	11386892
Bitter pills, bad medicine.	2001-06-04	11432381
"Diet pills" and major depression in the Canadian population.	2001-06	11441784
3,4-Methylenedioxymethamphetamine (MDMA) as a unique model of serotonin receptor function and serotonin-dopamine interactions.	2001-06	11356903
Transcranial magnetic stimulation and antidepressive drugs share similar cellular effects in rat hippocampus.	2001-06	11331140
Serotonin transporter promoter polymorphism is associated with attenuated prolactin response to fenfluramine.	2001-05-08	11378851
By the way, doctor...I used a diet pill--fenfluramine--a few years ago, but stopped as soon as I heard about it causing heart-valve problems. My doctor has been doing echocardiograms on me every six months. So far, everything looks good. How long do you think I need to keep on getting these checkups?	2001-05	11424276
Stress hormone dysregulation at rest and after serotonergic stimulation among alcohol-dependent men with extended abstinence and controls.	2001-05	11411461
Rapid clot formation and abnormal fibrin structure in a symptomatic patient taking fenfluramine--a case report.	2001-05	11386389
Decreased tryptophan availability but normal post-synaptic 5-HT2c receptor sensitivity in chronic fatigue syndrome.	2001-05	11352361
Effects of repeated systemic administration of d-Fenfluramine on serotonin and glutamate release in rat ventral hippocampus: comparison with methamphetamine using in vivo microdialysis.	2001-04	11330336
The quest for biological correlates of social phobia: an interim assessment.	2001-04	11328236
Understanding the neurobiology of suicidal behavior.	2001	11747126
Neuroendocrine responses to fenfluramine and its relationship to personality in alcoholism.	2001	11716144
High-speed liquid chromatography/tandem mass spectrometry using a monolithic column for high-throughput bioanalysis.	2001	11404848
Neurotransmitter and hormonal background of hostility in anorexia nervosa.	2001	11340360

Patents

Sample Use Guides

In Vivo Use Guide

0.12–0.90 mg/kg/day

Route of Administration: Oral

In Vitro Use Guide

Rat midbrain slices were used to make intracellular recordings from dopaminergic neurons of the substantia nigra and the ventral tegmental area. Gamma-aminobutyric acid (GABA)-mediated synaptic transmission was assessed from the inhibitory postsynaptic potentials (IPSPs) mediated by GABAA and GABAB receptors. Intracellular recordings from midbrain SNpc and VTA dopaminergic neurons were performed at 33.0 +/- 0.5°C in a recording chamber submerged with aCSF flowing at a rate of 2.5–3 mL•min-1 and continuously oxygenated, on the stage of an upright (inverted) microscope (Axioscope FS, Zeiss, Gottingen, Germany), equipped for infrared video microscopy (Hamamatsu, Tokyo, Japan) in order to allow a direct visualization of the recorded cells. Neurons, selected for their morphology, were identified as dopaminergic by their electrophysiological properties such as the presence of a regular spontaneous firing activity (0.5–4 Hz), a large inward current (Ih) in response to hyperpolarizing voltages and a membrane hyperpolarization due to dopamine (10–30 mmol•L-1) application . The recording electrodes were filled with 2 mol•L-1 KCl and had a tip resistance of 30–80 MW. GABAB synaptic potentials were evoked using a bipolar tungsten stimulating electrode with a tip separation of 300–700 mkm. Representative recordings showing the effect of fenfluramine in reducing the GABAB-mediated IPSP. Such effects were evident at concentrations below 1 mmol•L-1. The amplitude of synaptic potentials was halved by fenfluramine at concentration around 10 mmol•L-1 and was completely blocked by CGP (1 mmol•L-1), a selective GABAB receptor antagonist. Fenfluramine and sibutramine induce a concentration-dependent reduction of the GABAB-mediated inhibitory postsynaptic potentials (IPSPs).

Substance Class	Chemical Created by `admin` on `Mon Mar 31 18:25:43 GMT 2025` Edited by `admin` on `Mon Mar 31 18:25:43 GMT 2025`
Record UNII	3KC089243P
Record Status	`Validated (UNII)`
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Name

Type

Language

FENFLURAMINE HYDROCHLORIDE

Official Name

English

GANAL

Preferred Name

English

FENFLURAMINE HYDROCHLORIDE [USAN]

Common Name

English

FENFLURAMINE HYDROCHLORIDE [ORANGE BOOK]

Common Name

English

N-ETHYL-.ALPHA.-METHYL-M-(TRIFLUOROMETHYL)PHENETHYLAMINE HYDROCHLORIDE

Systematic Name

English

HHR-965

Code

English

FENFLURAMINE HYDROCHLORIDE [MI]

Common Name

English

(±)-FENFLURAMINE HYDROCHLORIDE

Common Name

English

BENZENEETHANAMINE, N-ETHYL-.ALPHA.-METHYL-3-(TRIFLUOROMETHYL)-, HYDROCHLORIDE

Systematic Name

English

2-ETHYLAMINO-1-(3-TRIFLUOROMETHYLPHENYL)PROPANE HYDROCHLORIDE

Systematic Name

English

Fenfluramine hydrochloride [WHO-DD]

Common Name

English

DL-FENFLURAMINE HYDROCHLORIDE

Common Name

English

FENFLURAMINE HYDROCHLORIDE [JAN]

Common Name

English

BENZENEETHANAMINE, N-ETHYL-.ALPHA.-METHYL-3-(TRIFLUOROMETHYL)-, HYDROCHLORIDE (1:1)

Systematic Name

English

FENFLURAMINE HYDROCHLORIDE [VANDF]

Common Name

English

RACEMIC FENFLURAMINE HYDROCHLORIDE

Common Name

English

N-ETHYL-.ALPHA.-METHYL-3-(TRIFLUOROMETHYL)BENZENEETHANAMINE HYDROCHLORIDE

Systematic Name

English

FENFLURAMINE HYDROCHLORIDE [MART.]

Common Name

English

AHR-3002

Code

English

FINTEPLA

Brand Name

English

FENFLURAMINE HCL

Common Name

English

Classification Tree Code System Code

NCI_THESAURUS

C29728