Iptakalim hydrochloride, a lipophilic para-amino compound, is a novel ATP-sensitive potassium channel (K ATP ) opener, as well as an α 4 β 2 -containing nicotinic acetylcholine receptor (nAChR) antagonist. In Vitro Iptakalim (Ipt) hydrochloride has been shown to reverse pulmonary resistance vascular remodeling, inhibit proliferation of pulmonary arterial smooth muscle cells (PASMCs) and airway smooth muscle cells (ASMCs), as well as protect PAECs from pathological stimulation. Iptakalim has an inhibitory effect on [Ca 2+ ]cyt increase and the proliferation of pulmonary arterial SMCs induced by endothelin-1 through activation of K ATP channels. Iptakalim (10 μM, 10 min) pretreatment of pulmonary arterial SMCs significantly prevents ransient ncrease of [Ca 2+ ]cyt elicited by endothelin-1. Iptakalim at he concentrations of 0.1, 1, and 10 AM lowered[3H]thymidine incorporation by 19.75±4.60% (n=10), 41.20±9.49% (n=10), and 54.74±10.11% (n=10), respectively, compared with that of cells treated only with endothelin-1. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo Iptakalim (10-60 mg/kg) attenuates nicotine-evoked conditioned responding. Iptakalim also attenuates chamber activity in these nicotine test sessions. .\nIptakalim (60 mg/kg) pretreatment significantly reduced activity (LSD comparisons). . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Thirty male Sprague-Dawley rats weighing 275-299 grams. Dosage: 0, 10, 30, or 60 mg/kg. Administration: IP, 10 min before the start of a 4-min test session. Result: Decreased chamber activity. Dipper entries following pretreatment with 30 and 60 mg/kg Iptakalim were significantly lower than with 0 (saline) or 10 mg/kg iptakalim pretreatment (Tukey HSD tests). Form:Solid