Jump to content

Blonanserin: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
Monkbot (talk | contribs)
Bots
3,695,952 edits
m →top: Task 16: replaced (1×) / removed (0×) deprecated |dead-url= and |deadurl= with |url-status=;
OAbot (talk | contribs)
Bots
438,441 edits
m Open access bot: doi added to citation with #oabot.
Line 50: Line 50:
Blonanserin acts as a mixed [[5-HT2A receptor|5-HT<sub>2A</sub>]] (K<sub>i</sub> = 0.812 nM) and [[D2 receptor|D<sub>2</sub> receptor]] (K<sub>i</sub> = 0.142&nbsp;nM) [[receptor antagonist|antagonist]] and also exerts some blockade of [[alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]]s (K<sub>i</sub> = 26.7&nbsp;nM).<ref name = NDT>{{cite journal|title=Profile of blonanserin for the treatment of schizophrenia|journal=Neuropsychiatric Disease and Treatment|year=2013|volume=9|pages=587–594|doi=10.2147/NDT.S34433|pmid=23766647|author1=Tenjin, T |author2=Miyamoto, S |author3=Ninomiya, Y |author4=Kitajima, R |author5=Ogino, S |author6=Miyake, N |author7=Yamaguchi, N |pmc=3677929}}</ref><ref name="pmid8093723">{{cite journal |vauthors=Oka M, Noda Y, Ochi Y, etal | title = Pharmacological profile of AD-5423, a novel antipsychotic with both potent dopamine-D2 and serotonin-S2 antagonist properties | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 264 | issue = 1 | pages = 158–65 |date=January 1993 | pmid = 8093723 | doi = | url = http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=8093723}}</ref> Blonanserin also shows significant affinity for the [[Dopamine receptor D3|D<sub>3</sub> receptor]] (K<sub>i</sub> = 0.494 nM).<ref name=hida>{{cite journal|last1=Hida|first1=H|last2=Mouri|first2=A|last3=Mori|first3=K|last4=Matsumoto|first4=Y|last5=Seki|first5=T|last6=Taniguchi|first6=M|last7=Yamada|first7=K|last8=Iwamoto|first8=K|last9=Ozaki|first9=N|last10=Nabeshima|first10=T|last11=Noda|first11=Y|title=Blonanserin Ameliorates Phencyclidine-Induced Visual-Recognition Memory Deficits: the Complex Mechanism of Blonanserin Action Involving D<sub>3</sub>-5-HT<sub>2A</sub> and D<sub>1</sub>-NMDA Receptors in the mPFC.|journal=Neuropsychopharmacology|date=14 August 2014|pmid=25120077|doi=10.1038/npp.2014.207|volume=40|issue=3|pages=601–13|pmc=4289947}}</ref> It lacks significant [[affinity (pharmacology)|affinity]] for numerous other sites including the [[5-HT1A receptor|5-HT<sub>1A</sub>]], [[5-HT3 receptor|5-HT<sub>3</sub>]], [[D1 receptor|D<sub>1</sub>]], [[alpha-2 adrenergic receptor|α<sub>2</sub>-adrenergic]], [[beta-adrenergic receptor|β-adrenergic]], [[H1 receptor|H<sub>1</sub>]], and [[muscarinic acetylcholine receptor|mACh receptor]]s and the [[monoamine transporter]]s,<ref name="pmid8093723"/> though it does possess low affinity for the [[sigma receptor]] (IC<sub>50</sub> = 286 nM).<ref name="pmid8093723"/>
Blonanserin acts as a mixed [[5-HT2A receptor|5-HT<sub>2A</sub>]] (K<sub>i</sub> = 0.812 nM) and [[D2 receptor|D<sub>2</sub> receptor]] (K<sub>i</sub> = 0.142&nbsp;nM) [[receptor antagonist|antagonist]] and also exerts some blockade of [[alpha-1 adrenergic receptor|α<sub>1</sub>-adrenergic receptor]]s (K<sub>i</sub> = 26.7&nbsp;nM).<ref name = NDT>{{cite journal|title=Profile of blonanserin for the treatment of schizophrenia|journal=Neuropsychiatric Disease and Treatment|year=2013|volume=9|pages=587–594|doi=10.2147/NDT.S34433|pmid=23766647|author1=Tenjin, T |author2=Miyamoto, S |author3=Ninomiya, Y |author4=Kitajima, R |author5=Ogino, S |author6=Miyake, N |author7=Yamaguchi, N |pmc=3677929}}</ref><ref name="pmid8093723">{{cite journal |vauthors=Oka M, Noda Y, Ochi Y, etal | title = Pharmacological profile of AD-5423, a novel antipsychotic with both potent dopamine-D2 and serotonin-S2 antagonist properties | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 264 | issue = 1 | pages = 158–65 |date=January 1993 | pmid = 8093723 | doi = | url = http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=8093723}}</ref> Blonanserin also shows significant affinity for the [[Dopamine receptor D3|D<sub>3</sub> receptor]] (K<sub>i</sub> = 0.494 nM).<ref name=hida>{{cite journal|last1=Hida|first1=H|last2=Mouri|first2=A|last3=Mori|first3=K|last4=Matsumoto|first4=Y|last5=Seki|first5=T|last6=Taniguchi|first6=M|last7=Yamada|first7=K|last8=Iwamoto|first8=K|last9=Ozaki|first9=N|last10=Nabeshima|first10=T|last11=Noda|first11=Y|title=Blonanserin Ameliorates Phencyclidine-Induced Visual-Recognition Memory Deficits: the Complex Mechanism of Blonanserin Action Involving D<sub>3</sub>-5-HT<sub>2A</sub> and D<sub>1</sub>-NMDA Receptors in the mPFC.|journal=Neuropsychopharmacology|date=14 August 2014|pmid=25120077|doi=10.1038/npp.2014.207|volume=40|issue=3|pages=601–13|pmc=4289947}}</ref> It lacks significant [[affinity (pharmacology)|affinity]] for numerous other sites including the [[5-HT1A receptor|5-HT<sub>1A</sub>]], [[5-HT3 receptor|5-HT<sub>3</sub>]], [[D1 receptor|D<sub>1</sub>]], [[alpha-2 adrenergic receptor|α<sub>2</sub>-adrenergic]], [[beta-adrenergic receptor|β-adrenergic]], [[H1 receptor|H<sub>1</sub>]], and [[muscarinic acetylcholine receptor|mACh receptor]]s and the [[monoamine transporter]]s,<ref name="pmid8093723"/> though it does possess low affinity for the [[sigma receptor]] (IC<sub>50</sub> = 286 nM).<ref name="pmid8093723"/>


Blonanserin has a relatively high affinity towards the [[5-HT6 receptor|5-HT<sub>6</sub> receptor]] perhaps underpinning its recently unveiled efficacy in treating the cognitive symptoms of schizophrenia.<ref name = NDT/><ref>{{cite journal|title=Effect of blonanserin on cognitive function in antipsychotic-naïve first-episode schizophrenia|journal=Human Psychopharmacology|date=January 2012|volume=27|issue=1|pages=90–100|doi=10.1002/hup.1276|pmid=22278973|author1=Tenjin, T |author2=Miyamoto, S |author3=Miyake, N |author4=Ogino, S |author5=Kitajima, R |author6=Ojima, K |author7=Arai, J |author8=Teramoto, H |author9=Tsukahara, S |author10=Ito, Y |author11=Tadokoro, M |author12=Anai, K |author13=Funamoto, Y |author14=Kaneda, Y |author15=Sumiyoshi, T |author16=Yamaguchi, N }}</ref> The efficacy of blonanserin can in part be attributed to its chemical structure, which is unique from those of other atypical antipsychotics.<ref name=suzuki>{{cite journal|last1=Suzuki|first1=K|last2=Hiyama|first2=Y|last3=Une|first3=T|last4=Fujiwara|first4=I|title=Crystal structure of an antipsychotic agent, 2-(4-ethyl-1-piperazinyl)-4-(4-fluorophenyl)-5,6,7,8,9,10-hexahydrocycloocta[b]pyridine (blonanserin).|journal=Analytical Sciences|date=November 2002|volume=18|issue=11|pages=1289–90|pmid=12458724|doi=10.2116/analsci.18.1289}}</ref> 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.<ref>{{cite journal|last1=Ochi|first1=T|last2=Sakamoto|first2=M|last3=Minamida|first3=A|last4=Suzuki|first4=K|last5=Ueda|first5=T|last6=Une|first6=T|last7=Toda|first7=H|last8=Matsumoto|first8=K|last9=Terauchi|first9=Y|title=Syntheses and properties of the major hydroxy metabolites in humans of blonanserin AD-5423, a novel antipsychotic agent.|journal=Bioorganic & Medicinal Chemistry Letters|date=15 February 2005|volume=15|issue=4|pages=1055–9|pmid=15686911|doi=10.1016/j.bmcl.2004.12.028}}</ref>
Blonanserin has a relatively high affinity towards the [[5-HT6 receptor|5-HT<sub>6</sub> receptor]] perhaps underpinning its recently unveiled efficacy in treating the cognitive symptoms of schizophrenia.<ref name = NDT/><ref>{{cite journal|title=Effect of blonanserin on cognitive function in antipsychotic-naïve first-episode schizophrenia|journal=Human Psychopharmacology|date=January 2012|volume=27|issue=1|pages=90–100|doi=10.1002/hup.1276|pmid=22278973|author1=Tenjin, T |author2=Miyamoto, S |author3=Miyake, N |author4=Ogino, S |author5=Kitajima, R |author6=Ojima, K |author7=Arai, J |author8=Teramoto, H |author9=Tsukahara, S |author10=Ito, Y |author11=Tadokoro, M |author12=Anai, K |author13=Funamoto, Y |author14=Kaneda, Y |author15=Sumiyoshi, T |author16=Yamaguchi, N }}</ref> The efficacy of blonanserin can in part be attributed to its chemical structure, which is unique from those of other atypical antipsychotics.<ref name=suzuki>{{cite journal|last1=Suzuki|first1=K|last2=Hiyama|first2=Y|last3=Une|first3=T|last4=Fujiwara|first4=I|title=Crystal structure of an antipsychotic agent, 2-(4-ethyl-1-piperazinyl)-4-(4-fluorophenyl)-5,6,7,8,9,10-hexahydrocycloocta[b]pyridine (blonanserin).|journal=Analytical Sciences|date=November 2002|volume=18|issue=11|pages=1289–90|pmid=12458724|doi=10.2116/analsci.18.1289|doi-access=free}}</ref> 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.<ref>{{cite journal|last1=Ochi|first1=T|last2=Sakamoto|first2=M|last3=Minamida|first3=A|last4=Suzuki|first4=K|last5=Ueda|first5=T|last6=Une|first6=T|last7=Toda|first7=H|last8=Matsumoto|first8=K|last9=Terauchi|first9=Y|title=Syntheses and properties of the major hydroxy metabolites in humans of blonanserin AD-5423, a novel antipsychotic agent.|journal=Bioorganic & Medicinal Chemistry Letters|date=15 February 2005|volume=15|issue=4|pages=1055–9|pmid=15686911|doi=10.1016/j.bmcl.2004.12.028}}</ref>


{| class="wikitable sortable"
{| class="wikitable sortable"

Revision as of 21:35, 11 April 2020

Blonanserin
Clinical data
Trade namesLonasen
Routes of
administration		By mouth
ATC code
  • none
Legal status
Legal status
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability55%[1]
MetabolismCYP3A4[1]
Elimination half-life12 h[1]
Excretion59% (urine), 30% (faeces)[1]
Identifiers
  • 2-(4-ethylpiperazin-1-yl)-4-(4-fluorophenyl)-5,6,7,8,9,10-hexahydrocycloocta[b]pyridine
CAS Number
PubChem CID
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.211.656 Edit this at Wikidata
Chemical and physical data
FormulaC23H30FN3
Molar mass367.50 g/mol g·mol−1
3D model (JSmol)
  • Fc1ccc(cc1)c2cc(nc3c2CCCCCC3)N4CCN(CC)CC4

Blonanserin, sold under the brand name 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 uses

Blonanserin is used to treat schizophrenia in Japan and South Korea but not in the US.[6]

Adverse 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]

Pharmacology

Pharmacodynamics

Blonanserin acts as a mixed 5-HT2A (Ki = 0.812 nM) and D2 receptor (Ki = 0.142 nM) antagonist and also exerts some blockade of α1-adrenergic receptors (Ki = 26.7 nM).[7][8] Blonanserin also shows significant affinity for the D3 receptor (Ki = 0.494 nM).[9] It lacks significant affinity for numerous other sites including the 5-HT1A, 5-HT3, D1, α2-adrenergic, β-adrenergic, H1, and mACh receptors and the monoamine transporters,[8] though it does possess low affinity for the sigma receptor (IC50 = 286 nM).[8]

Blonanserin has a relatively high affinity towards the 5-HT6 receptor perhaps underpinning its recently unveiled efficacy in treating the cognitive symptoms of schizophrenia.[7][10] The efficacy of blonanserin can in part be attributed to its chemical structure, which is unique from those of other atypical antipsychotics.[11] 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.[12]

Receptor Ki [nM] (Blonanserin)* [7] Ki [nM] (N-deethylblonanserin)* [3]
D1 1070 1020
D2 0.142 1.38
D3 0.494 0.23
D4 150 -
D5 2600 -
5-HT1A 804 -
5-HT2A 0.812 1.28
5-HT2C 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.

Action at the Dopamine-D3 receptor

Blonanserin has antagonistic action at dopamine-D3 receptors 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.[9][13] Olanzapine does not appear to affect PKA activity.[9][14] Many antipsychotics, such as haloperidol, chlorpromazine, risperidone and olanzapine primarily antagonize serotonin 5-HT2A and dopamine-D2 receptors and lack known action at dopamine-D2/3 receptors.[9][11]

Blonanserin Cartoon
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).[9][13]

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.[15] The drug is absorbed by a two compartment (central and peripheral) model with first-order absorption and elimination.[16] The half-life of blonanserin is dependent on the dose. A single dose of 4 mg has a half-life of 7.7 ± 4.63 h and a single dose of 8 mg has a half-life of 11.9 ± 4.3 h.[15] 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.[15]

Blonanserin is not a charged compound and exhibits very little chemical polarity. The polar surface area of Blonanserin is 19.7 Å[17] 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.[18]

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 = 9500 L, Vd periphery = 8650 L) although it is slower to absorb into the central compartment.[16]

Blonanserin does not meet the criteria in Lipinski's rule of five.[17]

Effects of food intake

Food intake slows the absorption of blonanserin and increases the bioavailability peripherally relative to centrally.[16] 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.[15]

See also

References

  1. ^ 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.
  2. ^ "Archived copy" (PDF). Archived from the original (PDF) on 2013-01-19. Retrieved 2013-08-16.{{cite web}}: CS1 maint: archived copy as title (link)
  3. ^ 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.
  4. ^ Heading CE (November 1998). "AD-5423 (Dainippon Pharmaceutical Co Ltd)". IDrugs : The Investigational Drugs Journal. 1 (7): 813–7. PMID 18465651.
  5. ^ a b Kishi, T; Matsuda, Y; Nakamura, H; Iwata, N (Feb 2013). "Blonanserin for schizophrenia: Systematic review and meta-analysis of double-blind, randomized, controlled trials". Journal of Psychiatric Research. 47 (2): 149–54. doi:10.1016/j.jpsychires.2012.10.011. PMID 23131856.
  6. ^ 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. doi:10.1097/wnf.0b013e3182aa38c4. PMID 24201235.
  7. ^ 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. PMC 3677929. PMID 23766647.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  8. ^ 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.
  9. ^ 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-HT2A and D1-NMDA Receptors in the mPFC". Neuropsychopharmacology. 40 (3): 601–13. doi:10.1038/npp.2014.207. PMC 4289947. PMID 25120077.
  10. ^ 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.
  11. ^ 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. 18 (11): 1289–90. doi:10.2116/analsci.18.1289. PMID 12458724.
  12. ^ 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. doi:10.1016/j.bmcl.2004.12.028. PMID 15686911.
  13. ^ 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. doi:10.1038/sj.bjp.0704608. PMC 1573270. PMID 11906969.
  14. ^ 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. doi:10.1097/00001756-200302100-00023. PMID 12598744.
  15. ^ a b c d 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. doi:10.1007/s40261-013-0167-9. PMID 24399453.
  16. ^ a b c 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. doi:10.1002/hup.2290. PMID 23417765.
  17. ^ a b "Properties Viewer"..
  18. ^ 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. doi:10.1097/jcp.0b013e3182825bce. PMID 23422369.


Retrieved from "https://en.wikipedia.org/w/index.php?title=Blonanserin&oldid=950395406"