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	C12H16F3N
Molecular Weight	231.2573
Charge	0
Count

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

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

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 Fenfluramine was introduced on the U.S. market in 1973 and withdrawn in 1997.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 The drug was withdrawn from the U.S. market in 1997 after reports of heart valve disease and pulmonary hypertension, including a condition known as cardiac fibrosis. It was subsequently withdrawn from other markets around the world.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 1430

Conditions

Condition	Modality	Highest Phase	Product
Obesity 203 Sources: http://www.rxlist.com/pondimin-drug/indications-dosage.htm	Primary	Approved 8429	Pondimin Approved Use Unknown
Epilepsy 121 Sources: https://clinicaltrials.gov/ct2/show/NCT02655198	Primary	Phase II 1132	Pondimin Approved Use Unknown
Lennox gastaut syndrome 2 Sources: https://clinicaltrials.gov/ct2/show/NCT02655198	Primary	Phase II 1132	Pondimin Approved Use Unknown
Dravet syndrome 5 Sources: https://clinicaltrials.gov/ct2/show/NCT02682927	Primary	Phase III 656	Pondimin Approved Use Unknown
Seizure disorders 4 Sources: https://clinicaltrials.gov/ct2/show/NCT02682927	Primary	Phase III 656	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 n = 1 Health Status: unhealthy Condition: Valsalva's maneuver Age Group: 11 years Sex: F Population Size: 1 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) n = 13 Health Status: unhealthy Condition: Lennox‐Gastaut syndrome (LGS) Age Group: 11.7 ± 4.4 years (range: 3‐17 years) Sex: M+F Population Size: 13 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 n = 40 Health Status: unhealthy Sex: unknown Population Size: 40 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) n = 13 Health Status: unhealthy Condition: Lennox‐Gastaut syndrome (LGS) Age Group: 11.7 ± 4.4 years (range: 3‐17 years) Sex: M+F Population Size: 13 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 n = 40 Health Status: unhealthy Sex: unknown Population Size: 40 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/212102s000lbl.pdf

Overview

CYP3A4	CYP2C9	CYP2D6	hERG
inhibitor 1587 inducer 781	substrate 1037 inhibitor 1767 inducer 389	substrate 1217 inhibitor 1852 inducer 97

OverviewOther

Other Inhibitor	Other Substrate	Other Inducer
CYP1A2 1524 CYP2B6 810 CYP2C8 911 CYP2C19 1478 P-gp 1461 BCRP 699 OATP1B1 788 OATP1B3 706 OAT1 599 OAT3 642 OCT2 647 MATE1 306 MATE2 263	CYP1A2 1054 CYP2B6 664 CYP2C19 991 CYP3A4/5 85 OAT3 339 OCT2 355 MATE1 135 MATE2 96 BCRP 561 OAT1 326	CYP1A2 701 CYP2B6 547 CYP2C8 168 CYP2C19 293

Drug as perpetrator

Target	Modality	Activity	Metabolite
BCRP 773	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 773	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP1A2 1692	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1A2 1692	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP1A2 1692	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2B6 1001	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2B6 1001	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2B6 1001	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2C19 1553	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C19 1553	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C19 1553	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2C8 965	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C8 965	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C8 965	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2C9 1819	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C9 1819	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2C9 1819	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2D6 1891	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2D6 1891	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP2D6 1891	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP3A4 1925	inducer 1573 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP3A4 1925	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
CYP3A4 1925	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE1 308	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE1 308	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE2 263	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE2 263	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT1 603	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT1 603	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT3 644	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT3 644	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OATP1B1 803	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OATP1B1 803	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OATP1B3 715	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OATP1B3 715	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OCT2 648	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OCT2 648	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
P-gp 1650	inhibitor 3277 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
P-gp 1650	inhibitor 3277 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 1037	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	minor
CYP2C19 991	substrate 3367 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 85	substrate 3367 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 561	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
BCRP 561	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE1 135	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE1 135	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
MATE2 96	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
MATE2 96	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT1 326	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT1 326	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OAT3 339	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OAT3 339	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
OCT2 355	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no
OCT2 355	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	no	NORFENFLURAMINE 2
CYP2D6 1217	substrate 3367 Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2020/212102Orig1s000ClinPharmR.pdf#page=6 Page: 6.0	yes
CYP1A2 1054	substrate 3367 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 664	substrate 3367 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
Nav1.5 100	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
[Development of pulmonary hypertension and multi-valvular damage caused by appetite depressants].	1998 Dec 1	10911459
Echocardiographic improvement over time after cessation of use of fenfluramine and phentermine.	1999 Dec	10593346
The promotion effect of anorectic drugs on aflatoxin B(1)-induced hepatic preneoplastic foci.	1999 Sep	10469626
[Anorectics and pulmonary hypertension].	2000 Feb 16	10838744
Dose and duration of fenfluramine-phentermine therapy impacts the risk of significant valvular heart disease.	2000 Jul 1	10867106
Understanding the neurobiology of suicidal behavior.	2001	11747126
High-speed liquid chromatography/tandem mass spectrometry using a monolithic column for high-throughput bioanalysis.	2001	11404848
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 Apr	11330336
Neuroendocrine serotonergic and dopaminergic responsivity in male schizophrenic patients during treatment with neuroleptics and after switch to risperidone.	2001 Aug	11512043
Hypothalamo-pituitary-adrenal axis dysfunction in chronic fatigue syndrome, and the effects of low-dose hydrocortisone therapy.	2001 Aug	11502777
Fenfluramine-induced pulmonary vasoconstriction: role of serotonin receptors and potassium channels.	2001 Aug	11457791
"Diet pills" and major depression in the Canadian population.	2001 Jun	11441784
3,4-Methylenedioxymethamphetamine (MDMA) as a unique model of serotonin receptor function and serotonin-dopamine interactions.	2001 Jun	11356903
Fluorometric determination of DL-fenfluramine, DL-norfenfluramine and phentermine in plasma by achiral and chiral high-performance liquid chromatography.	2001 Nov 5	11710586
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 Oct	11559922
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 Sep	11605076

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 `Fri Dec 15 16:20:58 GMT 2023` Edited by `admin` on `Fri Dec 15 16:20:58 GMT 2023`
Record UNII	3KC089243P
Record Status	`Validated (UNII)`
Record Version

Download

Name

Type

Language

FENFLURAMINE HYDROCHLORIDE

Official 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

GANAL

Brand Name

English

AHR-3002

Code

English

FINTEPLA

Brand Name

English

FENFLURAMINE HCL

Common Name

English

Classification Tree Code System Code

NCI_THESAURUS

C29728