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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/09/21 05:53:55」(JST)

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Blonanserin (Lonasen) is a relatively new atypical antipsychotic (approved by PMDA in January 2008)^[2] commercialized by Dainippon Sumitomo Pharma in Japan and Korea for the treatment of schizophrenia.^[3] Relative to many other antipsychotics, blonanserin has an improved tolerability profile, lacking side effects such as extrapyramidal symptoms, excessive sedation, or hypotension.^[4] As with many second-generation (atypical) antipsychotics it is significantly more efficacious in the treatment of the negative symptoms of schizophrenia compared to first-generation (typical) antipsychotics such as haloperidol.^[5]

Medical Use

The use of atypical antipsychotics as a first-line treatment for schizophrenia is controversial. The National Institute of Mental Health’s CATIE trials suggest that atypical antipsychotics are not significantly more effective against negative symptoms of schizophrenia than typical antipsychotics.^[6]^[7]^[8]^[9] Blonanserin contradicts these findings by demonstrating more efficacy in treating negative symptoms than the related atypical antipsychotic haloperidol.^[10] Despite its suggested advantages, blonanserin does not meet the criteria for Lipinski’s rule, indicating it may not have effective pharmacological or biological activity and predicting that it would not be successful in the clinical trial phases of drug development. Blonanserin is approved for treatment of schizophrenia in Japan and South Korea.^[11] Blonanserin is not approved for the same use by the FDA.^[11]

Pharmacodynamics

Blonanserin acts as a mixed 5-HT_2A (K_i = 0.812 nM) and D₂ receptor (K_i = 0.142 nM) antagonist and also exerts some blockade of α₁-adrenergic receptors (K_i = 26.7 nM).^[12]^[13] Blonanserin also shows significant affinity for the D₃ receptor (K_i = 0.494nM).^[14] It lacks significant affinity for numerous other sites including the 5-HT_1A, 5-HT₃, D₁, α₂-adrenergic, β-adrenergic, H₁, and mACh receptors and the monoamine transporters,^[13] though it does possess low affinity for the sigma receptor (IC₅₀ = 286 nM).^[13]

Blonanserin has a relatively high affinity towards the 5-HT₆ receptor perhaps underpinning its recently unveiled efficacy in treating the cognitive symptoms of schizophrenia.^[12]^[15] The efficacy of blonanserin can in part be attributed to its chemical structure, which is unique from those of other atypical antipsychotics.^[16] Specifically, the addition of hydroxyl groups to blonanserin's unique eight membered ring results in the (R) stereoisomer of the compound demonstrating increased affinity for the indicated targets.^[17]

Receptor	K_i [nM] (Blonanserin)* ^[12]	K_i [nM] (N-deethylblonanserin)* ^[3]
D₁	1070	1020
D₂	0.142	1.38
D₃	0.494	0.23
D₄	150	-
D₅	2600	-
5-HT_1A	804	-
5-HT_2A	0.812	1.28
5-HT_2C	26.4	4.50
5-HT₆	11.7	5.03
5-HT₇	183	-
α₁	26.7 (Rat brain)	206 (Rat receptor)
α₂	530 (Rat cloned)	-
M₁	100	-
H₁	765	-

* Towards human receptors unless otherwise specified.

Pharmacokinetics

Blonanserin is administered 4 mg orally 2 times a day or 8 mg once a day, for an adult male with a body mass index between 19–24 kg/m2 and a body weight equal to or greater than 50 kg.^[18] The drug is absorbed by a two compartment (central and peripheral) model with first-order absorption and elimination.^[19] The half-life of blonanserin is dependent on the dose. A single dose of 4 mg has a half-life of 7.7 ± 4.63h and a single dose of 8 mg has a half-life of 11.9 ± 4.3h.^[18] The increase of half-life with dose is possibly attributed to there being more individual concentration per time points below the lower limit necessary for quantification in the lower single dose.^[18]

Blonanserin is not a charged compound and exhibits very little chemical polarity. The polar surface area of Blonanserin is 19.7 Å^[20] It is commonly accepted that a compound needs to have polar surface area less than 90 Å to cross the blood brain barrier so blonanserin is expected to be quite permeable as is demonstrated by a high brain/ plasma ratio of 3.88.^[21]

Due to the good permeability of blonanserin, the volume of distribution in the central nervous system is greater than that in the periphery (Vd central = 9500L, Vd periphery = 8650L) although it is slower to absorb into the central compartment.^[19]

Despite some promising clinical trials^[18]^[19] blonanserin has not met the criteria for Lipinski's rule.^[20] A factor contributing to blonanserin’s failure to meet Lipinksi’s rule is that it has a relatively high molecular mass and successful lead compounds are expected to have a molecular mass less than 300g/mol.

Effect of Feeding

Food intake slows the absorption of blonanserin and increases the bioavailability peripherally relative to centrally.^[19] Single fasting doses are safe and the effects of feeding intake are possibly explained by an interaction between blonanserin and Cytochrome P450 3A4 in the gut.^[18]

Action at the Dopamine-D₃ receptor

The unique indication of blonanserin is antagonistic action at dopamine-D₃ receptors (link edit) in the medial prefrontal cortex that potentiates phosphorylation levels of Protein kinase A (PKA) and counteracts decreased activity at the dopamine-D₁ and/or NMDA receptors, thus potentiating GABA induced Cl- currents and resulting in improvements in cognitive performance.^[14]^[22] Similar atypical antipsychotics, such as olanzapine, fail to show comparable efficacy to rescue PKA activity.^[14]^[23] Previously identified atypical antipsychotics, such as haloperidol, chlorpromazine, risperidone and olanzapine primarily antagonize serotonin 5-HT2A and dopamine-D₂ receptors and lack known action at dopamine-D_2/3 receptors.^[14]^[16]


Blonanserin action at dopamine-D₃ receptor. Cartoon of blonanserin's antagonistic impact at the dopamine-D₃ receptor, reversing inhibition of PKA activity (also regulated by dopamine-D₁ and NMDA activity) thus potentiating GABA induced Cl- current. Inset illustrates uninterrupted dopamine (DA) activity at the dopamine-D₃ receptor. Inspired by Hida et al. (2014) and Yokota et al. (2002).^[14]^[22]

Side Effects

As with many of the atypical antipsychotics, blonanserin can elicit cardio metabolic risks. While the side effects of blonanserin – such as weight gain, cholesterol and triglyceride levels, glucose levels and other blood lipid levels – do not differ greatly from other atypical antipsychotics, the specificity of blonanserin appears to elicit milder side effects, with less weight gain in particular.^[5]

References

^ ^a ^b ^c ^d Wen, YG; Shang, DW; Xie, HZ; Wang, XP; Ni, XJ; Zhang, M; Lu, W; Qiu, C; Liu, X; Li, FF; Li, X; Luo, FT (March 2013). "Population pharmacokinetics of blonanserin in Chinese healthy volunteers and the effect of the food intake". Human Psychopharmacology 28 (2): 134–141. doi:10.1002/hup.2290. PMID 23417765.
^ http://www.pmda.go.jp/english/service/pdf/list/NewdrugsFY2007.pdf
^ ^a ^b Deeks, ED; Keating, GM (January 2010). "Blonanserin A Review of its Use in the Management of Schizophrenia". CNS Drugs 24 (1): 65–84. doi:10.2165/11202620-000000000-00000. PMID 20030420.
^ Heading CE (November 1998). "AD-5423 (Dainippon Pharmaceutical Co Ltd)". IDrugs : the Investigational Drugs Journal 1 (7): 813–7. PMID 18465651.
^ ^a ^b Kishi T, Matsuda Y, Nakamura H, Iwata N. Blonanserin for schizophrenia: Systematic review and meta-analysis of double-blind, randomized, controlled trials. Journal of Psychiatric Research [Internet]. 2013 Feb [cited 2013 Aug 17];47(2) 149–54. Available from: http://www.sciencedirect.com/science/article/pii/S002239561200324X
^ Manschreck, TC; Boshes, RA (2007). "The CATIE schizophrenia trial: results, impact, controversy.". Harvard review of psychiatry 15 (5): 245–58. PMID 17924259.
^ Lieberman, JA (October 2006). "Comparative effectiveness of antipsychotic drugs. A commentary on: Cost Utility Of The Latest Antipsychotic Drugs In Schizophrenia Study (CUtLASS 1) and Clinical Antipsychotic Trials Of Intervention Effectiveness (CATIE).". Archives of general psychiatry 63 (10): 1069–72. PMID 17015808.
^ Kane, JM (May 2006). "Commentary on the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE).". The Journal of clinical psychiatry 67 (5): 831–2. PMID 16841634.
^ McEvoy, JP (July 2006). "An overview of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study.". CNS spectrums 11 (7 Suppl 7): 4–8. PMID 16816794.
^ Garcia, E; Robert, M; Peris, F; Nakamura, H; Sato, N; Terazawa, Y (2009). "The efficacy and safety of blonanserin compared with haloperidol in acute-phase schizophrenia: a randomized, double-blind, placebo-controlled, multicentre study.". CNS drugs 23 (7): 615–25. PMID 19552488.
^ ^a ^b Wang, SM; Han, C; Lee, SJ; Patkar, AA; Masand, PS; Pae, CU (2013). "Asenapine, blonanserin, iloperidone, lurasidone, and sertindole: distinctive clinical characteristics of 5 novel atypical antipsychotics.". Clinical neuropharmacology 36 (6): 223–38. PMID 24201235.
^ ^a ^b ^c Tenjin, T; Miyamoto, S; Ninomiya, Y; Kitajima, R; Ogino, S; Miyake, N; Yamaguchi, N (2013). "Profile of blonanserin for the treatment of schizophrenia". Neuropsychiatric Disease and Treatment 9: 587–594. doi:10.2147/NDT.S34433. PMID 23766647.
^ ^a ^b ^c Oka M, Noda Y, Ochi Y et al. (January 1993). "Pharmacological profile of AD-5423, a novel antipsychotic with both potent dopamine-D2 and serotonin-S2 antagonist properties". The Journal of Pharmacology and Experimental Therapeutics 264 (1): 158–65. PMID 8093723.
^ ^a ^b ^c ^d ^e Hida, H; Mouri, A; Mori, K; Matsumoto, Y; Seki, T; Taniguchi, M; Yamada, K; Iwamoto, K; Ozaki, N; Nabeshima, T; Noda, Y (14 August 2014). "Blonanserin Ameliorates Phencyclidine-Induced Visual-Recognition Memory Deficits: the Complex Mechanism of Blonanserin Action Involving D₃-5-HT_2A and D₁-NMDA Receptors in the mPFC.". Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. PMID 25120077.
^ Tenjin, T; Miyamoto, S; Miyake, N; Ogino, S; Kitajima, R; Ojima, K; Arai, J; Teramoto, H; Tsukahara, S; Ito, Y; Tadokoro, M; Anai, K; Funamoto, Y; Kaneda, Y; Sumiyoshi, T; Yamaguchi, N (January 2012). "Effect of blonanserin on cognitive function in antipsychotic-naïve first-episode schizophrenia". Human Psychopharmacology 27 (1): 90–100. doi:10.1002/hup.1276. PMID 22278973.
^ ^a ^b Suzuki, K; Hiyama, Y; Une, T; Fujiwara, I (November 2002). "Crystal structure of an antipsychotic agent, 2-(4-ethyl-1-piperazinyl)-4-(4-fluorophenyl)-5,6,7,8,9,10-hexahydrocycloocta[b]pyridine (blonanserin).". Analytical sciences : the international journal of the Japan Society for Analytical Chemistry 18 (11): 1289–90. PMID 12458724.
^ Ochi, T; Sakamoto, M; Minamida, A; Suzuki, K; Ueda, T; Une, T; Toda, H; Matsumoto, K; Terauchi, Y (15 February 2005). "Syntheses and properties of the major hydroxy metabolites in humans of blonanserin AD-5423, a novel antipsychotic agent.". Bioorganic & medicinal chemistry letters 15 (4): 1055–9. PMID 15686911.
^ ^a ^b ^c ^d ^e Chen, X; Wang, H; Jiang, J; Chen, R; Zhou, Y; Zhong, W; Liu, H; Hu, P (March 2014). "The pharmacokinetic and safety profiles of blonanserin in healthy Chinese volunteers after single fasting doses and single and multiple postprandial doses.". Clinical drug investigation 34 (3): 213–22. PMID 24399453.
^ ^a ^b ^c ^d Wen, YG; Shang, DW; Xie, HZ; Wang, XP; Ni, XJ; Zhang, M; Lu, W; Qiu, C; Liu, X; Li, FF; Li, X; Luo, FT (March 2013). "Population pharmacokinetics of blonanserin in Chinese healthy volunteers and the effect of the food intake.". Human psychopharmacology 28 (2): 134–41. PMID 23417765.
^ ^a ^b http://www.chemicalize.org/structure/#!mol=Blonanserin. Missing or empty |title= (help); Missing or empty |url= (help).
^ Tateno, A; Arakawa, R; Okumura, M; Fukuta, H; Honjo, K; Ishihara, K; Nakamura, H; Kumita, S; Okubo, Y (Apr 2013). "Striatal and extrastriatal dopamine D2 receptor occupancy by a novel antipsychotic, blonanserin: a PET study with [11C]raclopride and [11C]FLB 457 in schizophrenia.". Journal of clinical psychopharmacology 33 (2): 162–9. PMID 23422369.
^ ^a ^b Yokota, K; Tatebayashi, H; Matsuo, T; Shoge, T; Motomura, H; Matsuno, T; Fukuda, A; Tashiro, N (March 2002). "The effects of neuroleptics on the GABA-induced Cl- current in rat dorsal root ganglion neurons: differences between some neuroleptics.". British journal of pharmacology 135 (6): 1547–55. PMID 11906969.
^ Nagai, T; Noda, Y; Une, T; Furukawa, K; Furukawa, H; Kan, QM; Nabeshima, T (10 February 2003). "Effect of AD-5423 on animal models of schizophrenia: phencyclidine-induced behavioral changes in mice.". Neuroreport 14 (2): 269–72. PMID 12598744.

English Journal

Development of novel therapy of schizophrenia in children and adolescents.

Klein C1, Bespalov A.
Expert opinion on investigational drugs.Expert Opin Investig Drugs.2014 Nov;23(11):1531-40. doi: 10.1517/13543784.2014.933806. Epub 2014 Jun 27.
INTRODUCTION: Typical and atypical antipsychotics are efficacious treatments for early-onset schizophrenia (EOS) with very subtle differences in their efficacy. Therefore, when choosing an antipsychotic, the side-effect profile of the individual antipsychotic needs to be taken into account. There is
PMID 24970455

Blonanserin Ameliorates Phencyclidine-Induced Visual-Recognition Memory Deficits: the Complex Mechanism of Blonanserin Action Involving D3-5-HT2A and D1-NMDA Receptors in the mPFC.

Hida H1, Mouri A1, Mori K1, Matsumoto Y2, Seki T3, Taniguchi M1, Yamada K4, Iwamoto K5, Ozaki N5, Nabeshima T3, Noda Y1.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology.Neuropsychopharmacology.2014 Aug 14. doi: 10.1038/npp.2014.207. [Epub ahead of print]
Blonanserin differs from currently used serotonin 5-HT2A/dopamine-D2 receptor antagonists in that it exhibits higher affinity for dopamine-D2/3 receptors than for serotonin 5-HT2A receptors. We investigated the involvement of dopamine-D3 receptors in the effects of blonanserin on cognitive impairmen
PMID 25120077

A case report of blonanserin-induced hyponatremia.

Bavle A.
The Journal of neuropsychiatry and clinical neurosciences.J Neuropsychiatry Clin Neurosci.2014 Summer;26(3):E43. doi: 10.1176/appi.neuropsych.13080182.
PMID 25093786

Japanese Journal

透析患者における夜間せん妄にブロナンセリンが有用であった2症例

宮本和子,池田輝明
精神医学 53(11), 1103-1106, 2011-11
NAID 40019046637

肝性脳症によるせん妄状態にBlonanserinが奏効した1症例 (特集症状性を含む器質性精神障害の症例)

山下智子,和氣玲,宮岡剛 [他]
臨床精神医学 40(10), 1353-1357, 2011-10
NAID 40019022612

Related Pictures

★リンクテーブル★

リンク元

「ブロナンセリン」

Blonanserin
Systematic (IUPAC) name
	2-(4-ethylpiperazin-1-yl)-4-(4-fluorophenyl)-5,6,7,8,9,10-hexahydrocycloocta[b]pyridine
Clinical data
Trade names	Lonasen
Legal status	℞ (Prescription only);
Routes of; administration	Oral
Pharmacokinetic data
Bioavailability	55%.
Metabolism	CYP3A4
Biological half-life	12 h
Excretion	59% (urine), 30% (faeces)
Identifiers
CAS Registry Number	132810-10-7
ATC code	None
PubChem	CID: 125564
ChemSpider	111697
UNII	AQ316B4F8C
KEGG	D01176
ChEMBL	CHEMBL178803
Chemical data
Formula	C23H30FN3
Molecular mass	367.50 g/mol
	SMILES Fc1ccc(cc1)c2cc(nc3c2CCCCCC3)N4CCN(CC)CC4 ;

　　[★]

英: blonanserin
商: ロナセン
関: 精神神経用剤、非定型抗精神病薬

製品の治療学的・製剤学的特性

(1)ドパミンD2受容体(サブファミリーD2、D3)及びセロトニン5-HT2A受容体に選択的な結合活性を示し、拮抗的に作用する。
(2)統合失調症における幻覚・妄想などの陽性症状、情動的引きこもり・情動の平板化などの陰性症状に対して改善効果を示す。
(3)リスペリドン及びハロペリドールを対照薬とした二重盲検比較試験を実施し、リスペリドンとの比較試験では陽性・陰性症状評価尺度(PANSS)の合計スコア変化量、ハロペリドールとの比較試験では最終全般改善度の改善率を有効性主要評価項目として本剤の対照薬に対する非劣性が示された。
(4)国内臨床試験における最終全般改善度の改善率(中等度改善以上)は、二重盲検比較試験で55.4％(153/276例)、長期投与試験で52.4％(227/433例)であった。
(5)重大な副作用として、悪性症候群(Syndromemalin)、遅発性ジスキネジア、麻痺性イレウス、抗利尿ホルモン不適合分泌症候群(SIADH)、横紋筋融解症、無顆粒球症、白血球減少、肺塞栓症、深部静脈血栓症、肝機能障害が報告されている。

[PC-1] Wen, YG; Shang, DW; Xie, HZ; Wang, XP; Ni, XJ; Zhang, M; Lu, W; Qiu, C; Liu, X; Li, FF; Li, X; Luo, FT (March 2013). "Population pharmacokinetics of blonanserin in Chinese healthy volunteers and the effect of the food intake". Human Psychopharmacology 28 (2): 134–141. doi:10.1002/hup.2290. PMID 23417765.

[2] ttp://www.pmda.go.jp/english/service/pdf/list/NewdrugsFY2007.pdf

[CNS_Drugs-3] Deeks, ED; Keating, GM (January 2010). "Blonanserin A Review of its Use in the Management of Schizophrenia". CNS Drugs 24 (1): 65–84. doi:10.2165/11202620-000000000-00000. PMID 20030420.

[pmid18465651-4] Heading CE (November 1998). "AD-5423 (Dainippon Pharmaceutical Co Ltd)". IDrugs : the Investigational Drugs Journal 1 (7): 813–7. PMID 18465651.

[kishi-5] Kishi T, Matsuda Y, Nakamura H, Iwata N. Blonanserin for schizophrenia: Systematic review and meta-analysis of double-blind, randomized, controlled trials. Journal of Psychiatric Research [Internet]. 2013 Feb [cited 2013 Aug 17];47(2) 149–54. Available from: http://www.sciencedirect.com/science/article/pii/S002239561200324X

[6] Manschreck, TC; Boshes, RA (2007). "The CATIE schizophrenia trial: results, impact, controversy.". Harvard review of psychiatry 15 (5): 245–58. PMID 17924259.

[7] Lieberman, JA (October 2006). "Comparative effectiveness of antipsychotic drugs. A commentary on: Cost Utility Of The Latest Antipsychotic Drugs In Schizophrenia Study (CUtLASS 1) and Clinical Antipsychotic Trials Of Intervention Effectiveness (CATIE).". Archives of general psychiatry 63 (10): 1069–72. PMID 17015808.

[8] Kane, JM (May 2006). "Commentary on the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE).". The Journal of clinical psychiatry 67 (5): 831–2. PMID 16841634.

[9] McEvoy, JP (July 2006). "An overview of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study.". CNS spectrums 11 (7 Suppl 7): 4–8. PMID 16816794.

[10] Garcia, E; Robert, M; Peris, F; Nakamura, H; Sato, N; Terazawa, Y (2009). "The efficacy and safety of blonanserin compared with haloperidol in acute-phase schizophrenia: a randomized, double-blind, placebo-controlled, multicentre study.". CNS drugs 23 (7): 615–25. PMID 19552488.

[name-11] Wang, SM; Han, C; Lee, SJ; Patkar, AA; Masand, PS; Pae, CU (2013). "Asenapine, blonanserin, iloperidone, lurasidone, and sertindole: distinctive clinical characteristics of 5 novel atypical antipsychotics.". Clinical neuropharmacology 36 (6): 223–38. PMID 24201235.

[NDT-12] Tenjin, T; Miyamoto, S; Ninomiya, Y; Kitajima, R; Ogino, S; Miyake, N; Yamaguchi, N (2013). "Profile of blonanserin for the treatment of schizophrenia". Neuropsychiatric Disease and Treatment 9: 587–594. doi:10.2147/NDT.S34433. PMID 23766647.

[pmid8093723-13] Oka M, Noda Y, Ochi Y et al. (January 1993). "Pharmacological profile of AD-5423, a novel antipsychotic with both potent dopamine-D2 and serotonin-S2 antagonist properties". The Journal of Pharmacology and Experimental Therapeutics 264 (1): 158–65. PMID 8093723.

[hida-14] Hida, H; Mouri, A; Mori, K; Matsumoto, Y; Seki, T; Taniguchi, M; Yamada, K; Iwamoto, K; Ozaki, N; Nabeshima, T; Noda, Y (14 August 2014). "Blonanserin Ameliorates Phencyclidine-Induced Visual-Recognition Memory Deficits: the Complex Mechanism of Blonanserin Action Involving D₃-5-HT_2A and D₁-NMDA Receptors in the mPFC.". Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. PMID 25120077.

[15] Tenjin, T; Miyamoto, S; Miyake, N; Ogino, S; Kitajima, R; Ojima, K; Arai, J; Teramoto, H; Tsukahara, S; Ito, Y; Tadokoro, M; Anai, K; Funamoto, Y; Kaneda, Y; Sumiyoshi, T; Yamaguchi, N (January 2012). "Effect of blonanserin on cognitive function in antipsychotic-naïve first-episode schizophrenia". Human Psychopharmacology 27 (1): 90–100. doi:10.1002/hup.1276. PMID 22278973.

[suzuki-16] Suzuki, K; Hiyama, Y; Une, T; Fujiwara, I (November 2002). "Crystal structure of an antipsychotic agent, 2-(4-ethyl-1-piperazinyl)-4-(4-fluorophenyl)-5,6,7,8,9,10-hexahydrocycloocta[b]pyridine (blonanserin).". Analytical sciences : the international journal of the Japan Society for Analytical Chemistry 18 (11): 1289–90. PMID 12458724.

[17] Ochi, T; Sakamoto, M; Minamida, A; Suzuki, K; Ueda, T; Une, T; Toda, H; Matsumoto, K; Terauchi, Y (15 February 2005). "Syntheses and properties of the major hydroxy metabolites in humans of blonanserin AD-5423, a novel antipsychotic agent.". Bioorganic & medicinal chemistry letters 15 (4): 1055–9. PMID 15686911.

[chen-18] Chen, X; Wang, H; Jiang, J; Chen, R; Zhou, Y; Zhong, W; Liu, H; Hu, P (March 2014). "The pharmacokinetic and safety profiles of blonanserin in healthy Chinese volunteers after single fasting doses and single and multiple postprandial doses.". Clinical drug investigation 34 (3): 213–22. PMID 24399453.

[wen-19] Wen, YG; Shang, DW; Xie, HZ; Wang, XP; Ni, XJ; Zhang, M; Lu, W; Qiu, C; Liu, X; Li, FF; Li, X; Luo, FT (March 2013). "Population pharmacokinetics of blonanserin in Chinese healthy volunteers and the effect of the food intake.". Human psychopharmacology 28 (2): 134–41. PMID 23417765.

[chem-20] http://www.chemicalize.org/structure/#!mol=Blonanserin. Missing or empty |title= (help); Missing or empty |url= (help).

[21] Tateno, A; Arakawa, R; Okumura, M; Fukuta, H; Honjo, K; Ishihara, K; Nakamura, H; Kumita, S; Okubo, Y (Apr 2013). "Striatal and extrastriatal dopamine D2 receptor occupancy by a novel antipsychotic, blonanserin: a PET study with [11C]raclopride and [11C]FLB 457 in schizophrenia.". Journal of clinical psychopharmacology 33 (2): 162–9. PMID 23422369.

[yokota-22] Yokota, K; Tatebayashi, H; Matsuo, T; Shoge, T; Motomura, H; Matsuno, T; Fukuda, A; Tashiro, N (March 2002). "The effects of neuroleptics on the GABA-induced Cl- current in rat dorsal root ganglion neurons: differences between some neuroleptics.". British journal of pharmacology 135 (6): 1547–55. PMID 11906969.

[23] Nagai, T; Noda, Y; Une, T; Furukawa, K; Furukawa, H; Kan, QM; Nabeshima, T (10 February 2003). "Effect of AD-5423 on animal models of schizophrenia: phencyclidine-induced behavioral changes in mice.". Neuroreport 14 (2): 269–72. PMID 12598744.

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案内

blonanserin