Corrigendum to "N-[(3S)-Pyrrolidin-3-yl]benzamides as novel dual serotonin and noradrenaline reuptake inhibitors: Impact of small structural modifications on P-gp recognition and CNS penetration" [Bioorg. Med. Chem. Lett. 19 (2009) 5078] (DOI:10.1016/j.bmcl.2009.07.049);N-[(3S)-Pyrrolidin-3-yl]benzamides as novel dual serotonin and noradrenaline reuptake inhibitors: Impact of small structural modifications on P-gp recognition and CNS penetration

Bioorganic and Medicinal Chemistry Letters

Volumn 19, Issue 17, 2009, Pages 5078-5081

  Wakenhut, Florian ^a   Allan, Gill A ^a   Fish, Paul V ^a   Jonathan Fray, M ^a   Harrison, Anthony C ^a   McCoy, Rachel ^a   Phillips, Stephen C ^a   Stobie, Alan ^a   Westbrook, Dominique ^a   Westbrook, Simon L ^a   Whitlock, Gavin A ^a  

^a PFIZER GLOBAL RESEARCH AND DEVELOPMENT   (United Kingdom)

Author keywords

CYP2D6 inhibition; MDCK mdr1; N (3S) Pyrrolidin 3 yl benzamides; Noradrenaline reuptake; P gp recognition; Serotonin reuptake; SNRI; Urinary incontinence

Indexed keywords

BENZAMIDE DERIVATIVE; GLYCOPROTEIN P; N (PYRROLIDIN 3 YL)BENZAMIDE DERIVATIVE; PF 184 298; SEROTONIN NORADRENALIN REUPTAKE INHIBITOR; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; DOG; DRUG BLOOD LEVEL; DRUG PENETRATION; DRUG POTENCY; DRUG SELECTIVITY; DRUG STABILITY; DRUG STRUCTURE; DRUG SYNTHESIS; ENZYME INHIBITION; FEMALE; HUMAN; HUMAN CELL; MAXIMUM PLASMA CONCENTRATION; NONHUMAN; PHYSICAL CHEMISTRY; STRESS INCONTINENCE; STRUCTURE ACTIVITY RELATION; STRUCTURE ANALYSIS;

ADRENERGIC UPTAKE INHIBITORS; ANILIDES; ANIMALS; BENZAMIDES; CELL LINE; CENTRAL NERVOUS SYSTEM; DOGS; DOPAMINE UPTAKE INHIBITORS; HUMANS; NOREPINEPHRINE; P-GLYCOPROTEIN; PYRROLIDINES; RATS; SEROTONIN UPTAKE INHIBITORS; STRUCTURE-ACTIVITY RELATIONSHIP;

EID: 68349150602     PISSN: 0960894X     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.bmcl.2009.11.096     Document Type: Erratum

References (26)

1. Jann M.W., and Slade J.H. Pharmacotherapy 11 (2007) 1571
2. Montgomery S. Int. J. Psych. Clin. Pract. 10 (2006) 5
3. Jackson S. Curr. Med. Res. Opin. 21 (2005) 1669
4. Wernicke J.F., Iyengar S., and Ferrer-Garcia M.D. Curr. Drug Ther. 2 (2007) 161
5. Bauer M., Moeller H.-J., and Schneider E. Exp. Opin. Pharmacotherapy 7 (2006) 421
6. Kajdasz D.K., Iyengar S., and Desaiah D. Clin. Ther. 29 (2007) 2536
7. Mariappan P., Alhasso A., Ballantyne Z., Grant A., and N'Dow J. Eur. Urol. 51 (2007) 67
8. Steers W.D., Herschorn S., Kreder K.J., Moore K., Strohbehn K., Yalcin I., and Bump R.C. BJU Int. 100 (2007) 337
9. Thor K.B., Kirby M., and Viktrup L. Int. J. Clin. Pract. 61 (2007) 1349
10. Fray M.J., Bish G., Brown A.D., Fish P.V., Stobie A., Wakenhut F., and Whitlock G.A. Bioorg. Med. Chem. Lett. 16 (2006) 4345
11. Fray M.J., Bish G., Fish P.V., Stobie A., Wakenhut F., and Whitlock G.A. Bioorg. Med. Chem. Lett. 16 (2006) 4349
12. Fish P.V., Fray M.J., Stobie A., Wakenhut F., and Whitlock G.A. Bioorg. Med. Chem. Lett. 17 (2007) 2022
13. Whitlock G.A., Blagg J., and Fish P.V. Bioorg. Med. Chem. Lett. 18 (2008) 596
14. Fish P.V., Deur C., Gan X., Greene K., Hoople D., Mackenny M., Para K.S., Reeves K., Ryckmans T., Stiff C., Stobie A., Wakenhut F., and Whitlock G.A. Bioorg. Med. Chem. Lett. 18 (2008) 2562
15. Wakenhut F., Fish P.V., Fray M.J., Gurrell I., Mills J.E., Stobie A., and Whitlock G.A. Bioorg. Med. Chem. Lett. 18 (2008) 4308
16. SNRI activity of target compounds was established using scintillation proximity assay (SPA) technology by assessing their ability to inhibit binding of selective radioligands at the human 5-HT, NA and DA transporters. Cellular membrane preparations generated from recombinant HEK293 cells expressing a single monoamine transporter were utilised for these experiments. For details of the assay conditions, see: Andrews, M. D.; Brown, A. D.; Fish, P. V.; Fray, M. J.; Lansdell, M. I.; Ryckmans, T.; Stobie, A.; Wakenhut, F.; Gray, D. L. F. WO Patent 064351, 2006, pp 56-59. The BioByte software was used to assess clog P.
17. Adult, female, nulliparous beagle dogs were anaesthetised initially with sodium pentobarbitone to induce surgical anaesthesia (30 mg/kg iv), and then transferred to α-chloralose anaesthetic (70-100 mg/kg iv induction followed by constant infusion to deliver 10-15 mg/kg/h iv for the duration of the experiment), following completion of surgery. Animals were intubated, and respiration maintained at a constant rate of 14 breaths per minute. Tidal volume was adjusted to maintain expired air within normal physiological limits. Throughout the experiment the animal was maintained at a core body temperature of approximately 37 °C using a thermocouple heated blanket (Harvard Apparatus Ltd., Kent, UK). Cannulation of superficial vessels was carried out to allow administration of compounds, blood sampling, infusion of anaesthetic, and monitoring of arterial pressure (Millar, 7F, Millar Instruments, US). A midline incision was made in the abdomen to expose the bladder. The ureters were cannulated to drain urine throughout the experiment. The dome of the bladder was cannulated and the cannula fed through the bladder to the external urethra. This catheter was used to introduce the urethral pressure catheter (Millar SUPC-380C), into the urethra. The bladder was filled with saline to achieve an intravesical pressure of approximately 8-10 mmHg, and bladder pressure was measured by connecting the bladder catheter to a pressure transducer (Model DTX plus, Becton-Dickenson UK Ltd, Oxford, UK). Following completion of surgery, animals were allowed to stabilise for at least 60 minutes before starting urethral pressure profilometry measurements. Urethral pressure profilometry (UPP) was measured by withdrawing the pressure transducer through the urethra at a constant rate. A full profile measurement was obtained approximately every 6 min, and readings were taken continuously throughout the experiment. Baseline measurements were performed until 4 consistent measurements were identified, after which drug administration commenced. From the profilometry data, peak urethral pressure was measured (PUP, mmHg). Changes in PUP were compared with mean baseline value and expressed as % change from baseline, recorded over the 4 consecutive profiles obtained prior to test drug or vehicle administration. All experiments involving animals were carried out in compliance with national legislation, specifically the UK Animal (Scientific Procedures) Act 1986, and subject to local ethical review.
18. Measuring CSF levels is commonly used as a way to assess Blood Brain Barrier penetration, see:. Lin L.H. Curr. Drug. Metab. 9 (2008) 46
19. Feng M.R. Curr. Drug. Metab. 3 (2002) 647
20. Deecher D.C., Beyer C.E., Johnston G., Bray J., Shah S., Abou-Gharbia M., and Andree T.H. J. Pharm. Exp. Ther. 318 (2006) 657
21. Mahar Doan K.M., Humphreys J.E., Webster L.O., Wring S.A., Shampine L.J., Serabjit-Singh C.J., Adkison K.K., and Polli J.W. J. Pharm. Exp. Ther. 303 (2002) 1029
22. The MDCK-mdr1 cell line is commonly used to assess P-gp recognition, see:. Hammarlund-Udenaes M., Bredberg U., and Friden M. Curr. Top. Med. Chem. 9 (2009) 148
23. For a substrate model of the P-gp transporter, see:. Seelig A. Eur. J. Biochem. 251 (1998) 252
24. Chan C., Yeo K.P., Pan A.X., Lim M., Knadler M.P., and Small D.S. Br J. Clin. Pharm. 63 (2006) 310
25. kinner M.H., Kuan H., Pan A., Sathirakul K., Knadler M.P., Gonzales C.R., Yeo K.P., Reddy S., Lim M., Ayan-Oshodi M., and Wise S.D. Clin. Pharm. Ther. 73 (2003) 170
26. For detailed experimental procedures see Supplementary data.