• cytoplasm • organelle membrane • integral component of membrane • cytoskeleton • endoplasmic reticulum membrane • endomembrane system • membrane
Biological process
• arachidonic acid metabolic process • fatty acid catabolic process
Sources:Amigo / QuickGO
Orthologs
Species
Human
Mouse
Entrez
2166
14073
Ensembl
ENSG00000117480
ENSMUSG00000034171
UniProt
O00519
O08914
RefSeq (mRNA)
NM_001441
NM_010173
RefSeq (protein)
NP_001432
NP_034303
Location (UCSC)
Chr 1: 46.39 – 46.41 Mb
Chr 4: 115.97 – 116.02 Mb
PubMed search
[3]
[4]
Wikidata
View/Edit Human
View/Edit Mouse
Fatty acid amide hydrolase or FAAH (EC 3.5.1.99, oleamide hydrolase, anandamide amidohydrolase) is a member of the serine hydrolase family of enzymes. It was first shown to break down anandamide in 1993.[5] In humans, it is encoded by the gene FAAH.[6][7][8]
Contents
1Function
2Inhibitors and inactivators
2.1Inhibition and binding
3Assays
4Structures
5See also
6References
7External links
Function
FAAH is an integral membrane hydrolase with a single N-terminal transmembrane domain. In vitro, FAAH has esterase and amidase activity.[9]In vivo, FAAH is the principal catabolic enzyme for a class of bioactive lipids called the fatty acid amides (FAAs). Members of the FAAs include:
Anandamide (N-arachidonoylethanolamine), an endocannabinoid[10]
2-arachidonoylglycerol (2-AG), an endocannabinoid.[11]
Other N-acylethanolamines, such as N-oleoylethanolamine and N-palmitoylethanolamine[12]
The sleep-inducing lipid oleamide[13]
The N-acyltaurines, which are agonists of the transient receptor potential (TRP) family of calcium channels.[14]
FAAH knockout mice display highly elevated (>15-fold) levels of N-acylethanolamines and N-acyltaurines in various tissues. Because of their significantly elevated anandamide levels, FAAH KOs have an analgesic phenotype, showing reduced pain sensation in the hot plate test, the formalin test, and the tail flick test.[15] Finally, because of their impaired ability to degrade anandamide, FAAH KOs also display supersensitivity to exogenous anandamide, a cannabinoid receptor (CB) agonist.[10]
Due to the ability of FAAH to regulate nociception, it is currently viewed as an attractive drug target for the treatment of pain.[16][17][18]
A mutation in FAAH was initially provisionally linked to drug abuse and dependence but this was not borne out in subsequent studies.[19]
Studies in cells and animals and genetic studies in humans have shown that inhibiting FAAH may be a useful strategy to treat anxiety disorders.[19][20][21]
Inhibitors and inactivators
Based on the hydrolytic mechanism of fatty acid amide hydrolase, a large number of irreversible and reversible inhibitors of this enzyme have been developed.[22][23][24][25][26][27][28][29]
Some of the more significant compounds are listed below;
AM374, palmitylsulfonyl fluoride, one of the first FAAH inhibitors developed for in vitro use, but too reactive for research in vivo
ARN2508, derivative of flurbiprofen, dual FAAH / COX inhibitor
BIA 10-2474 (Bial-Portela & Ca. SA, Portugal) has been linked to severe adverse events affecting 5 patients in a drug trial in Rennes, France, and at least one death, in January 2016.[30] Many other pharmaceutical companies have previously taken other FAAH inhibitors into clinical trials without reporting such adverse events.
BMS-469908[31]
CAY-10402
JNJ-245
JNJ-1661010[32]
JNJ-28833155
JNJ-40413269
JNJ-42119779
JNJ-42165279 in clinical trials against social anxiety and depression,[33] trials suspended as a precautionary measure following serious adverse event with BIA 10-2474[34]
LY-2183240 [35]
Cannabidiol[36]
MK-3168
MK-4409
MM-433593
OL-92
OL-135
PF-622
PF-750 [37]
PF-3845
PF-04457845 "exquisitely selective" for FAAH over other serine hydrolases, but failed in clinical trials against osteoarthritis[38]
PF-04862853
RN-450
SA-47
SA-73
SSR-411298 well tolerated in clinical trials but insufficient efficacy against depression, subsequently trialled against cancer pain as an adjunctive treatment.[39][40]
ST-4068, reversible inhibitor of FAAH
TK-25
URB524
URB597 (KDS-4103, Kadmus Pharmaceuticals), is an irreversible inactivator with a carbamate-based mechanism, and appears in one report as a somewhat selective, though it also inactivates other serine hydrolases (e.g., carboxylesterases) in peripheral tissues.[37]
URB694
URB937
VER-156084 (Vernalis)[41]
V-158866 (Vernalis) in clinical trials for neuropathic pain following spinal injury,[42] and spasticity associated with multiple sclerosis. Structure not revealed though Vernalis holds several patents in the area.[43][44]
Inhibition and binding
Structural and conformational properties that contribute to enzyme inhibition and substrate binding imply an extended bound conformation, and a role for the presence, position, and stereochemistry of a delta cis double bond.[45]
Assays
The enzyme is typically assayed making use of a radiolabelled anandamide substrate, which generates free labelled ethanolamine, although alternative LC-MS methods have also been described.[46][47]
Structures
The first crystal structure of FAAH was published in 2002 (PDB code 1MT5).[8] Structures of FAAH with drug-like ligands were first reported in 2008, and include non-covalent inhibitor complexes and covalent adducts.[48]
See also
Endocannabinoid enhancer
Endocannabinoid reuptake inhibitor
Monoacylglycerol lipase
FAAH2
References
^ abcGRCh38: Ensembl release 89: ENSG00000117480 - Ensembl, May 2017
^ abcGRCm38: Ensembl release 89: ENSMUSG00000034171 - Ensembl, May 2017
^Deutsch DG, Chin SA (September 1993). "Enzymatic synthesis and degradation of anandamide, a cannabinoid receptor agonist". Biochemical Pharmacology. 46 (5): 791–6. doi:10.1016/0006-2952(93)90486-G. PMID 8373432.
^Cravatt BF, Giang DK, Mayfield SP, Boger DL, Lerner RA, Gilula NB (November 1996). "Molecular characterization of an enzyme that degrades neuromodulatory fatty-acid amides". Nature. 384 (6604): 83–7. doi:10.1038/384083a0. PMID 8900284.
^Giang DK, Cravatt BF (March 1997). "Molecular characterization of human and mouse fatty acid amide hydrolases". Proceedings of the National Academy of Sciences of the United States of America. 94 (6): 2238–42. doi:10.1073/pnas.94.6.2238. PMC 20071. PMID 9122178.
^Patricelli MP, Cravatt BF (October 1999). "Fatty acid amide hydrolase competitively degrades bioactive amides and esters through a nonconventional catalytic mechanism". Biochemistry. 38 (43): 14125–30. doi:10.1021/bi991876p. PMID 10571985.
^ abCravatt BF, Demarest K, Patricelli MP, Bracey MH, Giang DK, Martin BR, Lichtman AH (July 2001). "Supersensitivity to anandamide and enhanced endogenous cannabinoid signaling in mice lacking fatty acid amide hydrolase". Proceedings of the National Academy of Sciences of the United States of America. 98 (16): 9371–6. doi:10.1073/pnas.161191698. PMC 55427. PMID 11470906.
^"The fatty acid amide hydrolase (FAAH)". Chemistry and Physics of Lipids. 108 (1–2): 107–121. 2000-11-01. doi:10.1016/S0009-3084(00)00190-0. ISSN 0009-3084.
^Saghatelian A, Trauger SA, Want EJ, Hawkins EG, Siuzdak G, Cravatt BF (November 2004). "Assignment of endogenous substrates to enzymes by global metabolite profiling". Biochemistry. 43 (45): 14332–9. doi:10.1021/bi0480335. PMID 15533037.
^Cravatt BF, Prospero-Garcia O, Siuzdak G, Gilula NB, Henriksen SJ, Boger DL, Lerner RA (June 1995). "Chemical characterization of a family of brain lipids that induce sleep". Science. 268 (5216): 1506–9. doi:10.1126/science.7770779. PMID 7770779.
^Saghatelian A, McKinney MK, Bandell M, Patapoutian A, Cravatt BF (August 2006). "A FAAH-regulated class of N-acyl taurines that activates TRP ion channels". Biochemistry. 45 (30): 9007–15. doi:10.1021/bi0608008. PMID 16866345.
^Cravatt BF, Lichtman AH (October 2004). "The endogenous cannabinoid system and its role in nociceptive behavior". Journal of Neurobiology. 61 (1): 149–60. doi:10.1002/neu.20080. PMID 15362158.
^Sałaga M, Sobczak M, Fichna J (2014). "Inhibition of fatty acid amide hydrolase (FAAH) as a novel therapeutic strategy in the treatment of pain and inflammatory diseases in the gastrointestinal tract". European Journal of Pharmaceutical Sciences. 52: 173–9. doi:10.1016/j.ejps.2013.11.012. PMID 24275607.
^Ulugöl A (2014). "The endocannabinoid system as a potential therapeutic target for pain modulation". Balkan Medical Journal. 31 (2): 115–20. doi:10.5152/balkanmedj.2014.13103. PMC 4115931. PMID 25207181.
^Ghosh S, Kinsey SG, Liu QS, Hruba L, McMahon LR, Grim TW, et al. (2015). "Full Fatty Acid Amide Hydrolase Inhibition Combined with Partial Monoacylglycerol Lipase Inhibition: Augmented and Sustained Antinociceptive Effects with Reduced Cannabimimetic Side Effects in Mice". The Journal of Pharmacology and Experimental Therapeutics. 354 (2): 111–20. doi:10.1124/jpet.115.222851. PMC 4518073. PMID 25998048.
^ abPanlilio LV, Justinova Z, Goldberg SR (2013). "Inhibition of FAAH and activation of PPAR: new approaches to the treatment of cognitive dysfunction and drug addiction". Pharmacology & Therapeutics. 138 (1): 84–102. doi:10.1016/j.pharmthera.2013.01.003. PMC 3662489. PMID 23333350.
^Gunduz-Cinar O, Hill MN, McEwen BS, Holmes A (November 2013). "Amygdala FAAH and anandamide: mediating protection and recovery from stress". Trends in Pharmacological Sciences. 34 (11): 637–44. doi:10.1016/j.tips.2013.08.008. PMC 4169112. PMID 24325918.
^Berardi A, Schelling G, Campolongo P (September 2016). "The endocannabinoid system and Post Traumatic Stress Disorder (PTSD): From preclinical findings to innovative therapeutic approaches in clinical settings". Pharmacological Research. 111: 668–78. doi:10.1016/j.phrs.2016.07.024. PMID 27456243.
^Janero DR, Vadivel SK, Makriyannis A (April 2009). "Pharmacotherapeutic modulation of the endocannabinoid signalling system in psychiatric disorders: drug-discovery strategies". International Review of Psychiatry (Abingdon, England). 21 (2): 122–33. doi:10.1080/09540260902782778. PMC 5531754. PMID 19367506.
^Ahn K, Johnson DS, Cravatt BF (July 2009). "Fatty acid amide hydrolase as a potential therapeutic target for the treatment of pain and CNS disorders". Expert Opinion on Drug Discovery. 4 (7): 763–784. doi:10.1517/17460440903018857. PMC 2882713. PMID 20544003.
^Petrosino S, Di Marzo V (January 2010). "FAAH and MAGL inhibitors: therapeutic opportunities from regulating endocannabinoid levels". Current Opinion in Investigational Drugs. 11 (1): 51–62. PMID 20047159.
^Minkkilä A, Saario S, Nevalainen T (2010). "Discovery and development of endocannabinoid-hydrolyzing enzyme inhibitors". Current Topics in Medicinal Chemistry. 10 (8): 828–58. doi:10.2174/156802610791164238. PMID 20370710.
^Khanna IK, Alexander CW (August 2011). "Fatty acid amide hydrolase inhibitors--progress and potential". CNS & Neurological Disorders Drug Targets. 10 (5): 545–58. doi:10.2174/187152711796234989. PMID 21631410.
^Bisogno T, Maccarrone M (May 2013). "Latest advances in the discovery of fatty acid amide hydrolase inhibitors". Expert Opinion on Drug Discovery. 8 (5): 509–22. doi:10.1517/17460441.2013.780021. PMID 23488865.
^Pertwee RG (February 2014). "Elevating endocannabinoid levels: pharmacological strategies and potential therapeutic applications". The Proceedings of the Nutrition Society. 73 (1): 96–105. doi:10.1017/S0029665113003649. PMID 24135210.
^Lodola A, Castelli R, Mor M, Rivara S (2015). "Fatty acid amide hydrolase inhibitors: a patent review (2009-2014)". Expert Opinion on Therapeutic Patents. 25 (11): 1247–66. doi:10.1517/13543776.2015.1067683. PMID 26413912.
^Enserink M (2016). "More Details Emerge on Fateful French Drug Trial" (online). Science (January 16). doi:10.1126/science.aae0247. Retrieved 16 January 2016.
^Min X, Thibault ST, Porter AC, Gustin DJ, Carlson TJ, Xu H, Lindstrom M, Xu G, Uyeda C, Ma Z, Li Y, Kayser F, Walker NP, Wang Z (May 2011). "Discovery and molecular basis of potent noncovalent inhibitors of fatty acid amide hydrolase (FAAH)". Proceedings of the National Academy of Sciences of the United States of America. 108 (18): 7379–84. doi:10.1073/pnas.1016167108. PMC 3088576. PMID 21502526.
^Keith JM, Jones WM, Tichenor M, Liu J, Seierstad M, Palmer JA, Webb M, Karbarz M, Scott BP, Wilson SJ, Luo L, Wennerholm ML, Chang L, Rizzolio M, Rynberg R, Chaplan SR, Breitenbucher JG (December 2015). "Preclinical Characterization of the FAAH Inhibitor JNJ-42165279". ACS Medicinal Chemistry Letters. 6 (12): 1204–8. doi:10.1021/acsmedchemlett.5b00353. PMC 4677372. PMID 26713105.
^"Janssen Research & Development, LLC Voluntarily Suspends Dosing in Phase 2 Clinical Trials of Experimental Treatment for Mood Disorders". Janssen.com. 17 January 2016. Retrieved 21 January 2016.
^Moore SA, Nomikos GG, Dickason-Chesterfield AK, Schober DA, Schaus JM, Ying BP, Xu YC, Phebus L, Simmons RM, Li D, Iyengar S, Felder CC (December 2005). "Identification of a high-affinity binding site involved in the transport of endocannabinoids". Proceedings of the National Academy of Sciences of the United States of America. 102 (49): 17852–7. doi:10.1073/pnas.0507470102. PMC 1295594. PMID 16314570.
^Campos AC, Moreira FA, Gomes FV, Del Bel EA, Guimarães FS (December 2012). "Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 367 (1607): 3364–78. doi:10.1098/rstb.2011.0389. PMC 3481531. PMID 23108553.
^ abAhn K, Johnson DS, Fitzgerald LR, Liimatta M, Arendse A, Stevenson T, Lund ET, Nugent RA, Nomanbhoy TK, Alexander JP, Cravatt BF (November 2007). "Novel mechanistic class of fatty acid amide hydrolase inhibitors with remarkable selectivity". Biochemistry. 46 (45): 13019–30. doi:10.1021/bi701378g. PMID 17949010.
^Fowler CJ (2015). "The Potential of Inhibitors of Endocannabinoid Metabolism for Drug Development: A Critical Review". Handbook of Experimental Pharmacology. Handbook of Experimental Pharmacology. 231: 95–128. doi:10.1007/978-3-319-20825-1_4. ISBN 978-3-319-20824-4. PMID 26408159.
^Clinical trial number NCT00822744 for "An Eight-week Study of SSR411298 as Treatment for Major Depressive Disorder in Elderly Patients (FIDELIO)" at ClinicalTrials.gov
^"Clinical trials for SSR411298". EU Clinical Trials Register.
^Clinical trial number NCT01748695 NCT01748695 for " A Safety, Tolerability and Efficacy Study of V158866 in Central Neuropathic Pain Following Spinal Cord Injury" at ClinicalTrials.gov
^US granted 8450346, "Azetidine derivatives as FAAH inhibitors", published 28 May 2013, assigned to Vernalis (R&D) Ltd.
^Roughley SD, Browne H, Macias AT, Benwell K, Brooks T, D'Alessandro J, et al. (January 2012). "Fatty acid amide hydrolase inhibitors. 3: tetra-substituted azetidine ureas with in vivo activity". Bioorganic & Medicinal Chemistry Letters. 22 (2): 901–6. doi:10.1016/j.bmcl.2011.12.032. PMID 22209458.
^Boger DL, Sato H, Lerner AE, Austin BJ, Patterson JE, Patricelli MP, Cravatt BF (January 1999). "Trifluoromethyl ketone inhibitors of fatty acid amide hydrolase: a probe of structural and conformational features contributing to inhibition". Bioorganic & Medicinal Chemistry Letters. 9 (2): 265–70. doi:10.1016/S0960-894X(98)00734-3. PMID 10021942.
^Wang Y, Jones P (2009). "A scintillation proximity assay for fatty acid amide hydrolase compatible with inhibitor screening". Methods in Molecular Biology. Methods in Molecular Biology. 572: 247–59. doi:10.1007/978-1-60761-244-5_16. ISBN 978-1-60761-243-8. PMID 20694697.
^Han B, Wright R, Kirchhoff AM, Chester JA, Cooper BR, Davisson VJ, Barker E (January 2013). "Quantitative LC-MS/MS analysis of arachidonoyl amino acids in mouse brain with treatment of FAAH inhibitor". Analytical Biochemistry. 432 (2): 74–81. doi:10.1016/j.ab.2012.09.031. PMC 3760509. PMID 23044255.
^PDB: 2VYA; Mileni M, Johnson DS, Wang Z, Everdeen DS, Liimatta M, Pabst B, Bhattacharya K, Nugent RA, Kamtekar S, Cravatt BF, Ahn K, Stevens RC (September 2008). "Structure-guided inhibitor design for human FAAH by interspecies active site conversion". Proceedings of the National Academy of Sciences of the United States of America. 105 (35): 12820–4. doi:10.1073/pnas.0806121105. PMC 2529035. PMID 18753625.
External links
fatty-acid+amide+hydrolase at the US National Library of Medicine Medical Subject Headings (MeSH)
Proteopedia FAAH entry - interactive structure (JMOL) of inhibitor-bound FAAH
v
t
e
Cannabinoid receptor modulators
Receptor (ligands)
CB1
Agonists(abridged; see here for more): 2-AG
2-AGE (noladin ether)
11-Hydroxy-THC
α-Amyrin
β-Amyrin
AB-CHMINACA
AM-1172
AM-1220
AM-1221
AM-1235
AM-2201
AM-2232
Anandamide
Arvanil
AZ-11713908
Cannabinol
CB-13
CP 47,497
CP 55,940
Dimethylheptylpyran
DEA
ECG
EGCG
Epicatechin
Gallocatechol (gallocatechin)
Honokiol
HU-210
JWH-007
JWH-015
JWH-018
JWH-073
Kavain
L-759,633
Levonantradol
Menabitan
Nabilone
Nabitan
NADA
O-1812
Oleamide
Pravadoline
Serinolamide A
THC (dronabinol)
UR-144
WIN 55,212-2
Yangonin
Antagonists: AM-251
AM-6545
Cannabidiol
Cannabigerol
Drinabant
Falcarinol (carotatoxin)
Hemopressin
Ibipinabant
LY-320,135
MK-9470
NESS-0327
O-2050
Otenabant
PF-514273
PipISB
Rimonabant
Rosonabant
Surinabant
Taranabant
THCV
TM-38837
VCHSR
Virodhamine
Antibodies: Brizantin (Бризантин)
Dietressa (Диетресса)
Unknown/unsorted: MAFP
CB2
Agonists: 2-AG
2-AGE (noladin ether)
3,3'-Diindolylmethane
4-O-Methylhonokiol
α-Amyrin
β-Amyrin
A-796,260
A-834,735
A-836,339
AM-1172
AM-1221
AM-1235
AM-1241
AM-2232
Anandamide
AZ-11713908
Cannabinol
Caryophyllene
CB-13
CBS-0550
CP-55,940
GW-405,833 (L-768,242)
GW-842,166X
HU-308
JTE 7-31
JWH-007
JWH-015
JWH-018
JWH-73
JWH-133
L-759,633
L-759,656
Lenabasum (anabasum)
Magnolol
MDA-19
Nabitan
NADA
Olorinab (APD-371)
PF-03550096
S-444,823
SER-601
Serinolamide A
UR-144
Tedalinab
THC (dronabinol)
THCV
Tetrahydromagnolol
Virodhamine
Antagonists: 4-O-Methylhonokiol
AM-630
BML-190
Cannabidiol
Honokiol
JTE-907
SR-144,528
WIN 54,461
WIN 56,098
NAGly (GPR18)
Agonists: Abnormal cannabidiol
ACPA
AM251
Anandamide
Cannabidiol
NADGly
THC (dronabinol)
O-1602
Antagonists: CID-85469571
O-1918
GPR55
Agonists: 2-AGE (noladin ether)
2-ALPI
Abnormal cannabidiol
AM-251
CID1011163
CID1252842
CID1792579
CP 55,940
GSK-494581A
Lysophosphatidylinositol
ML-184
ML-185
ML-186
O-1602
Oleoylethanolamide
Palmitoylethanolamide
THC (dronabinol)
Antagonists: Cannabidiol
CID-16020046
ML-191
ML-192
ML-193
O-1918
PSB-SB-487
PSB-SB-1202
PSB-SB-1203
Tetrahydromagnolol
GPR119
Agonists: 2-Oleoylglycerol
Anandamide
APD668
AR-231,453
AS-1269574
MBX-2982
N-Oleoyldopamine
Oleoylethanolamide
Olvanil
PSN-375,963
PSN-632,408
Unsorted
Agonists: Revosimeline
Transporter (modulators)
eCBTs
Inhibitors: 5'-DMH-CBD
AM-404
AM-1172
Arachidonoyl serotonin
Arvanil
Cannabidiol
Guineensine
LY-2183240
O-2093
OMDM-2
Paracetamol (acetaminophen)
SB-FI-26
UCM-707
URB-597
VDM-11
WOBE490
WOBE491
WOBE492
Enzyme (modulators)
FAAH
Inhibitors: 4-Nonylphenylboronic acid
AACOCF3
AM-404
Arachidonoyl serotonin
BIA 10-2474
Biochanin A
Genistein
IDFP
JNJ-1661010
JNJ-42165279
JZL-195
Kaempferol
LY-2183240
MAFP
Palmitoylisopropylamide
Paracetamol (acetaminophen)
PF-3845
PF-04457845
PF-750
SA-47
SA-57
TAK 21d
TC-F 2
UCM710
URB-597
Activators: PDP-EA
MAGL
Inhibitors: ABX-1431
IDFP
JJKK 048
JW 642
JZL-184
JZL-195
JZP-361
KML 29
MAFP
MJN110
NAM
Pristimerin
URB-602
ABHD6
Inhibitors: JZP-169
JZP-430
KT182
KT185
KT195
KT203
LEI-106
ML294
ML295
ML296
UCM710
WWL-70
ABHD12
Inhibitors: Betulinic acid
Maslinic acid
MAFP
Oleanolic acid
Orlistat (tetrahydrolipstatin)
Ursolic acid
Others
Precursors: Phosphatidylethanolamine
NAPE
Diacylglycerol
Others: 2-PG (directly potentiates activity of 2-AG at CB1 receptor)
This article is part of a series on Information security Related security categories Internet security Cyberwarfare Computer security Mobile security Network security Threats Computer crime Vulnerability Eavesdropping Malware Spyware Ransomware Trojans Viruses Worms Rootkits Bootkits Keyloggers Screen scrapers Exploits Backdoors Logic bombs Payloads Denial of service Defenses Computer access control Application security Antivirus software Secure coding Secure by default Secure by design Secure operating systems Authentication Multi-factor authentication Authorization Data-centric security Encryption Firewall Intrusion detection system Mobile secure gateway Runtime application self-protection (RASP) v t e Information security , sometimes shortened to InfoSec , is the practice of preventing unauthorized access, use, disclosure, disruption, modification, inspection, recording or destruction of information. Th...
For Lambak Kiri public housing area, see Lambak Kiri Landless Indigenous Citizens' Housing Scheme. Village in Brunei-Muara, Brunei Lambak Kiri Village Location in Brunei Coordinates: 4°59′26″N 114°57′04″E / 4.990472°N 114.951114°E / 4.990472; 114.951114 Coordinates: 4°59′26″N 114°57′04″E / 4.990472°N 114.951114°E / 4.990472; 114.951114 Country Brunei District Brunei-Muara Mukim Berakas A Government • Village head Hamdani Omar Postcode BB1214 Lambak Kiri is a populated place in Brunei-Muara District, Brunei. It is officially a village subdivision under Berakas A, a mukim in the district. Lambak Kiri may also refer to the greater area which includes the Lambak Kiri public housing area of the Landless Indigenous Citizens' Housing Scheme (Malay: Skim Tanah Kurnia Rakyat Jati ), although the latter is a separate subdivision. Contents 1 Name 2 Administration 3 See also 4 References Name ...
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