生物活性

• 描述Cilnidipine is a calcium channel blocker that blocks both L and N-type calcium channels and inhibits excessive release of norepinephrine from the sympathetic nerve ending. Cilnidipine which inhibits N-type calcium channels is more useful for patients with hypertension and diabetes mellitus from its effects on glucose and lipid metabolism and renal function^[3]. Cilnidipine selectively reduced only L-type HVA I(Ca) at the low concentrations under 10(-7) and 10(-6) M. Cilnidipine blocked not only L- but also N-type HVA I(Ca). At the high concentration over 10(-6) M cilnidipine non-selectively blocked the T-type LVA and P/Q- and R-type HVA Ca2+ channels^[4]. In the rat focal brain ischemia model, an anti-hypertensive and anti-sympathetic dose of cilnidipine could reduce the size of cerebral infarction, whereas an equipotent hypotensive dose of nilvadipine failed to affect it^[5]. Cilnidipine is more effective than amlodipine at improving renal function and arterial stiffness in patients with essential hypertension^[6]. Cilnidipine, a commercially available NTCC-blocking drug (N-type Ca2+-channels), prevents AF-induced autonomic, electrical and structural remodelling, along with associated AF (atrial fibrillation) promotion^[7]. Cilnidipine has an advantage of causing less reflex tachycardia, less pedal edema and better control of proteinuria in comparison to L-type CCB (calcium channel blocker). By causing dilatation of efferent arteriole, it causes less damage to glomeruli and suppresses podocyte injury. Cilnidipine also increases insulin sensitivity. Cilnidipine as CCB can be a good choice in hypertensive patients with diabetes, chronic kidney disease and in patients developing pedal edema with other CCB^[8].
• 临床研究

• NCT号	适应症或疾病	临床期	招募状态	预计完成时间	地点
  NCT00541853	Kidney, Polycystic, Autosomal ... more >>Dominant Collapse <<	Phase 4	Unknown	November 2012	Japan ... more >> Kyorin University School of Medicine Not yet recruiting Mitaka, Tokyo, Japan, 181-8611 Contact: Eiji Higashihara, M.D.    81+422475511 ext 5813    ehigashi@kyorin-u.ac.jp    Contact: Kikuo Nutahara, M.D.    81-422475511 ext 5815    kinuta@kyorin-u.ac.jp    Department of Urology, National Hospital Organaization Chiba-East Hospital Not yet recruiting Chiba, Chiba, Japan, 260-8712 Contact: Koichi Kamura, MD    81+432615171 ext 7607    kamura@cehpnet.com    Toranomon Hospital Kajigaya, Kidney center Not yet recruiting Kanagawa, Japan, 213-8587 Contact: Yoshifumi Ubara, MD    81+448775111 ext 6064    ubara@toranomon.gr.jp    Toranomon Hospital, Kidney center Not yet recruiting Tokyo, Japan, 105-8470 Contact: Kenmei Tkaichi, MD    81+335881111 ext 7065    takaichi@toranomon.gr.jp    Division of Kidney and Hypertension, Department of Internal Medicine, Jikei University School of Medicine Not yet recruiting Tokyo, Japan, 105-8471 Contact: Tatsuo Hosoya, MD    81+334331111 ext 3220    t-hosoya@jikei.ac.jp    Contact: Kazushige Hanaoka, MD    81+334331111 ext 3221    khanaoka@jikei.ac.jp    Department of Urology, Teikyo University, School of Medicine Not yet recruiting Tokyo, Japan, 173-8605 Contact: Shigeo Horie, MD    81+339641211    shorie@med.teikyo-u.ac.jp    Contact: Satoru Muto, MD    81+33964-1211    muto@med.teikyo-u.ac.jp Collapse <<
  NCT02145104	Hypertension	Phase 3	Completed	-	Korea, Republic of ... more >> Seoul National University Bundang Hospital Seongnam-si, Kyung-gi, Korea, Republic of Collapse <<
  NCT00890279	Kidney, Polycystic, Autosomal ... more >>Dominant Collapse <<	Phase 2	Unknown	November 2012	Japan ... more >> Department of Medicine II, Hokkaido Univserity School of Medicine Recruiting Sapporo, Hokkaido, Japan, 0608638 Contact: Toshio Mochizuki, MD    +81117065915    mtoshi@med.hokudai.ac.jp    Principal Investigator: Toshio Mochizuki, MD          Toranomon Hospital Kajigaya, Kidney center Not yet recruiting Kawasaki, Kanagawa, Japan, 2138587 Contact: Yoshihumi Ubara, MD    +81448775111 ext 6064    ubara@toranomon.gr.jp    Principal Investigator: Yoshihumi Ubara, MD          Department of Medicine II, Nippon Medical School Not yet recruiting Bunkyo-ku, Tokyo, Japan, 1138602 Contact: Yasuhiko Iino, MD    +81338222131    iinoyasuhiko@nms.ac.jp    Principal Investigator: Yasuhiko Iino, MD          Department of Urology, Teikyo University School of Medicine Recruiting Itabashi-ku, Tokyo, Japan, 1738605 Contact: Shigeo Horie, MD    +81339642497    shorie@med.teikyo-u.ac.jp    Contact: Satoru Muto, MD    +81339642497    muto@med.teikyo-u.ac.jp    Principal Investigator: Shigeo Horie, MD          Toranomon Hospital, Kidney center Not yet recruiting Minato-ku, Tokyo, Japan, 1058470 Contact: Kenmei Takaichi, MD    +81335881111 ext 7065    takaichi@toranomon.gr.jp    Principal Investigator: Kenmei Takaichi, MD          Division of Kidney and Hypertension, Department of Internal Medicine, Jikei University School of Medicine Active, not recruiting Minato-ku, Tokyo, Japan, 1058471 Department of Urology, Kyorin University School of Medicine Not yet recruiting Mitaka, Tokyo, Japan, 1818611 Contact: Eiji HIgashihara, MD    81422475511    ehigashi@kyorin-u.ac.jp    Contact: Kikuo Nutahara, MD    81422475511    kinuta@kyorin-u.ac.jp    Principal Investigator: Eiji Higashihara, MD          Sub-Investigator: Kikuo Nutahara, MD          Department of Urology, National Hospital Organaization Chiba-East Hospital Not yet recruiting Chiba, Japan, 2608712 Contact: Koichi Kamura, MD    +81432615171 ext 7607    kamura@cehpnet.com    Principal Investigator: Koichi Kamura, MD          Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences Not yet recruiting Niigata, Japan, 9518510 Contact: Ichiei Narita, MD    +813252272193    naritai@med.niigata-u.ac.jp    Principal Investigator: Ichiei Narita, MD Collapse <<

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• 参考文献

• [1] Takahara A, Fujita S, et al. Neuronal Ca2+ channel blocking action of an antihypertensive drug, cilnidipine, in IMR-32 human neuroblastoma cells. Hypertens Res. 2003 Sep;26(9):743-7.

  [2] Shiomi T, Tsutsui H, et al. Pioglitazone, a peroxisome proliferator-activated receptor-gamma agonist, attenuates left ventricular remodeling and failure after experimental myocardial infarction. Circulation. 2002 Dec 10;106(24):3126-32.

  [3] Masuda T, Ogura MN, Moriya T, et al. Beneficial effects of L- and N-type calcium channel blocker on glucose and lipid metabolism and renal function in patients with hypertension and type II diabetes mellitus. Cardiovasc Ther. 2011;29(1):46‐53

  [4] Murai Y, Uneyama H, Ishibashi H, Takahama K, Akaike N. Preferential inhibition of L- and N-type calcium channels in the rat hippocampal neurons by cilnidipine. Brain Res. 2000;854(1-2):6‐10

  [5] Takahara A, Konda T, Enomoto A, Kondo N. Neuroprotective effects of a dual L/N-type Ca(2+) channel blocker cilnidipine in the rat focal brain ischemia model. Biol Pharm Bull. 2004;27(9):1388‐1391

  [6] Morimoto S, Yano Y, Maki K, Iwasaka T. Renal and vascular protective effects of cilnidipine in patients with essential hypertension. J Hypertens. 2007;25(10):2178‐2183

  [7] Tajiri K, Guichard JB, Qi X, et al. An N-/L-type calcium channel blocker, cilnidipine, suppresses autonomic, electrical, and structural remodelling associated with atrial fibrillation. Cardiovasc Res. 2019;115(14):1975‐1985

  [8] Shete MM. Cilnidipine: Next Generation Calcium Channel Blocker. J Assoc Physicians India. 2016;64(4):95‐99

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