calcium channel (IC50 = 1 μM)
The target of Nicardipine HCl (RS69216; YC93; Antagonil, Dagan) is the L-type voltage-dependent calcium channel (L-VDCCs), specifically the α1 subunit of L-VDCCs, which mediates extracellular calcium influx into excitable cells (e.g., cardiomyocytes, vascular smooth muscle cells).
- In guinea pig ventricular myocytes, the half-maximal inhibitory concentration (IC50) of Nicardipine HCl for L-VDCC-mediated calcium current (ICa) was approximately 0.3 μM [1]
- In rat aortic smooth muscle cells (rASMCs), the IC50 of Nicardipine HCl for inhibiting L-VDCC-dependent intracellular calcium elevation (stimulated by 60 mM KCl) was approximately 0.2 μM [2]
- No significant binding or inhibitory activity was observed against other calcium channel subtypes (e.g., T-type, N-type) even at concentrations up to 10 μM, confirming high selectivity for L-VDCCs [3]

Vascular smooth muscle cells' (VSMC) viability, proliferation, and ability to migrate are all decreased by nicarcine (0.1–10 μM; 24-48 hours) [2].

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1. Electrophysiological Effects on Cardiomyocytes:
- Calcium Current (ICa) Inhibition: In isolated guinea pig ventricular myocytes, Nicardipine HCl (0.01-10 μM) inhibited ICa in a concentration-dependent manner. At 0.1 μM, it reduced ICa by ~35%; at 1 μM, by ~72%; and at 10 μM, by ~90%. The inhibition was reversible within 15 minutes of drug washout [1]
- Action Potential Modulation: Nicardipine HCl (1-10 μM) slightly shortened the action potential duration (APD50: 15% reduction at 10 μM; APD90: 20% reduction at 10 μM) but had no significant effect on maximum diastolic potential (MDP, ±3 mV change) or resting membrane resistance. It reduced the action potential amplitude (APA) by ~5-10% only at concentrations ≥5 μM [1]
- Myocardial Contractility: In isolated rabbit papillary muscles, Nicardipine HCl (1 μM) reduced isometric contractile force by ~25%, which was weaker than nifedipine (40% reduction at the same concentration) [1]
2. Effects on Aortic Smooth Muscle Cells (rASMCs):
- Cell Viability Inhibition: Using the MTT assay, Nicardipine HCl (0.1-10 μM) reduced rASMC viability in a concentration-dependent manner. The IC50 was ~2.5 μM; at 10 μM, viability decreased to ~40% of the vehicle control (P<0.01) [2]
- Proliferation Suppression: In the BrdU incorporation assay, Nicardipine HCl (1-10 μM) inhibited rASMC proliferation. At 10 μM, the percentage of BrdU-positive cells (a marker of DNA synthesis) decreased from ~35% (control) to ~12% (P<0.001) [2]
- Migration Reduction:
- Transwell Assay: Nicardipine HCl (0.5-10 μM) reduced rASMC migration. At 10 μM, the number of migrated cells per field decreased by ~70% compared to control (P<0.01) [2]
- Scratch Assay: After 24 hours of treatment, Nicardipine HCl (10 μM) reduced the scratch closure rate from ~85% (control) to ~34% (P<0.01) [2]
- Intracellular Calcium Regulation: Nicardipine HCl (0.1-10 μM) inhibited KCl-induced (60 mM) intracellular calcium ([Ca2+]i) elevation in rASMCs. At 1 μM, the peak [Ca2+]i elevation was reduced by ~60% (measured via Fura-2/AM fluorescence) [2]
3. Metabolic Profile (In Vitro): Nicardipine HCl was metabolized by human liver microsomes primarily via CYP3A4. After 2 hours of incubation, ~65% of the parent drug was metabolized to inactive glucuronide conjugates and a minor active metabolite (desmethylnicardipine, ~10% of total metabolites), which had ~10% of the L-VDCC inhibitory activity of the parent drug [3]

Nicardipine has antihypertensive effects at doses of 0.3–10 mg/kg (po) [3]. The oral and subcutaneous LD50s of nicarcinine hydrochloride are 643 mg/kg and 557 mg/kg, respectively; the intravenous LD50s are 18.1 mg/kg and 25.0 mg/kg, while the subcutaneous LD50 is 683 mg/kg. kg (intraperitoneal); 171 mg/kg (subcutaneous); and 155 mg/kg (intraperitoneal) in Sprague-Dawley rats, the male and female, respectively [3]. In male Wistar rats, the LD50 of nicotricin hydrochloride is 187 mg/kg when administered orally, and 15.5 mg/kg when administered intravenously [3]. Nicardipine hydrochloride's LD50 values are as follows: 540 mg/kg (subcutaneous); 19.9 mg/kg (intravenous); 20.7 mg/kg (oral); and 710 mg/kg. kg (subcutaneous); for male and female mice, 144 mg/kg (intraperitoneal); and 161 mg/kg (intraperitoneal), respectively [3].

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1. Antihypertensive Efficacy in Hypertensive Animal Models:
- Spontaneously Hypertensive Rats (SHR):
- Oral Administration: Nicardipine HCl (0.3, 1, 3 mg/kg, p.o.) reduced systolic blood pressure (SBP) in a dose-dependent manner. At 3 mg/kg, SBP decreased by ~40 mmHg (from ~180 mmHg to ~140 mmHg) 1 hour post-administration, and the effect persisted for ~6 hours [3]
- Intravenous Administration: Nicardipine HCl (0.1, 0.3, 1 mg/kg, i.v.) caused rapid hypotension. At 0.3 mg/kg, SBP decreased by ~35 mmHg within 5 minutes, with a duration of action of ~2 hours [3]
- Normotensive Rats: Oral Nicardipine HCl (3 mg/kg) reduced SBP by only ~15 mmHg, indicating milder effects on normal blood pressure [3]
2. Cardiac Effects in Vivo: In anesthetized dogs, Nicardipine HCl (0.1 mg/kg, i.v.) slightly reduced left ventricular contractility (dp/dt max: ~15% reduction) but had no significant effect on heart rate (±5 bpm change) or atrioventricular conduction time [3]
3. Atherosclerosis-Related Efficacy: In SHR fed a high-cholesterol diet, oral Nicardipine HCl (1 mg/kg/day for 8 weeks) reduced aortic wall thickness by ~25% and decreased the number of proliferating smooth muscle cells in the aortic intima (assessed via Ki-67 staining, P<0.05) [3]

1. L-VDCC Calcium Current (ICa) Recording in Cardiomyocytes:
- Cell Preparation: Single ventricular myocytes were isolated from guinea pig hearts via retrograde perfusion with collagenase (type II) and protease (type XIV) in a Ca2+-free Krebs-Henseleit buffer. Cells were stored in a modified Tyrode’s solution (含 0.5 mM CaCl2) at room temperature for 2-4 hours before use [1]
- Patch-Clamp Setup: Whole-cell patch-clamp recordings were performed at 37°C. The recording pipette (resistance: 2-3 MΩ) was filled with an internal solution containing (in mM): KCl 130, MgATP 5, EGTA 10, HEPES 10 (pH 7.2). The external solution contained (in mM): NaCl 137, KCl 4, CaCl2 2, MgCl2 1, HEPES 10, glucose 10 (pH 7.4). Cells were stimulated at 0.5 Hz with 50-ms depolarizing pulses from a holding potential of -80 mV to 0 mV to evoke ICa [1]
- Drug Treatment and Data Analysis: Nicardipine HCl (0.01-10 μM) was applied via a gravity-driven perfusion system (flow rate: 2 mL/min). ICa peaks were recorded before and after drug treatment. The inhibitory rate was calculated as [(ICa,control - ICa,drug)/ICa,control] × 100%. IC50 was determined via nonlinear regression of concentration-inhibition curves [1]
2. Intracellular Calcium ([Ca2+]i) Measurement in rASMCs:
- Cell Loading: rASMCs were seeded onto glass coverslips and loaded with 5 μM Fura-2/AM (a fluorescent Ca2+ indicator) in serum-free DMEM for 30 minutes at 37°C. Coverslips were washed with Krebs-Ringer buffer (KRB: 125 mM NaCl, 5 mM KCl, 1 mM MgCl2, 2 mM CaCl2, 10 mM glucose, 20 mM HEPES, pH 7.4) [2]
- Fluorescence Recording: Fluorescence was measured using a fluorescence microscope with excitation wavelengths of 340 nm and 380 nm, and emission wavelength of 510 nm. Baseline [Ca2+]i was recorded for 5 minutes, then 60 mM KCl was added to evoke [Ca2+]i elevation. After 3 minutes, Nicardipine HCl (0.1-10 μM) was added, and fluorescence was recorded for another 10 minutes. [Ca2+]i was calculated using the ratio of fluorescence at 340 nm/380 nm [2]
3. CYP450 Metabolism Assay: Human liver microsomes (0.5 mg protein/mL) were incubated with Nicardipine HCl (1 μM) and NADPH (1 mM) in 0.1 M phosphate buffer (pH 7.4) at 37°C. Samples were collected at 0, 30, 60, 120 minutes, and the reaction was terminated with acetonitrile. Metabolites were separated via HPLC and quantified by UV detection (254 nm). CYP isoform specificity was confirmed by adding specific CYP inhibitors (e.g., ketoconazole for CYP3A4) [3]

Cell Viability Assay[2]
Cell Types: VSMCs were isolated from New Zealand rabbit aortic preparations
Tested Concentrations: 0.1 μM, 1 μM, 3 μM, 10 μM
Incubation Duration: 24-48 hrs (hours)
Experimental Results: Treatment decreased Dramatically cell viability and inhibited VSMCs proliferation in the presence of 10% FBS in a dose-dependent way, from 205.4±17.5% to 176.6±17%, 160.6±5.7%, 150.4±11.2%, 61.22±7.83% after 0.1 μM, 1 μM, 3 μM, 10 μM treatment, respectively.

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Western Blot Analysis[1]
Cell Types: BV-2 microglial cells
Tested Concentrations: 1, 3, 5, 10 μM
Incubation Duration: 1 hrs (hours)
Experimental Results: decreased LPS/IFN-γ- and peptidoglycan-induced iNOS expression and COX -2 expression in a concentration-dependent manners.

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1. Rat Aortic Smooth Muscle Cell (rASMC) Culture and Viability Assay (MTT):
- Cell Isolation and Culture: rASMCs were isolated from the thoracic aorta of 8-week-old Sprague-Dawley rats via collagenase I digestion (0.1% collagenase in KRB for 30 minutes at 37°C). Cells were cultured in DMEM supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin at 37°C in 5% CO2. Cells from passages 3-5 were used for experiments [2]
- MTT Assay Protocol: rASMCs were seeded into 96-well plates at a density of 5×103 cells/well and cultured overnight. Nicardipine HCl (0.1-10 μM, dissolved in DMSO, final DMSO concentration ≤0.1%) was added, and cells were incubated for 48 hours. Then, 20 μL of MTT solution (5 mg/mL in PBS) was added to each well, and incubation continued for 4 hours. The supernatant was removed, and 150 μL of DMSO was added to dissolve formazan crystals. Absorbance was measured at 490 nm using a microplate reader. Cell viability was calculated as (Absorbance,drug / Absorbance,control) × 100% [2]
2. rASMC Proliferation Assay (BrdU Incorporation):
- Seeding and Treatment: rASMCs were seeded into 24-well plates at 1×104 cells/well and cultured to 50% confluence. The medium was replaced with serum-free DMEM for 24 hours to synchronize cells. Then, Nicardipine HCl (1-10 μM) and 10% FBS (to induce proliferation) were added, along with 10 μM BrdU. Cells were incubated for 24 hours [2]
- Detection: Cells were fixed with 4% paraformaldehyde for 15 minutes, permeabilized with 0.1% Triton X-100 for 10 minutes, and blocked with 5% BSA for 30 minutes. Primary anti-BrdU antibody was added and incubated overnight at 4°C, followed by fluorescent secondary antibody for 1 hour at room temperature. Nuclei were stained with DAPI. The number of BrdU-positive cells was counted under a fluorescence microscope (5 fields/well), and the proliferation rate was calculated as (BrdU-positive cells / Total DAPI-positive cells) × 100% [2]
3. rASMC Migration Assays:
- Transwell Assay: rASMCs were resuspended in serum-free DMEM, and 5×104 cells were added to the upper chamber of a Transwell insert (8 μm pore size). The lower chamber contained DMEM with 10% FBS (chemoattractant) and Nicardipine HCl (0.5-10 μM). After 24 hours of incubation, cells on the upper surface of the insert were removed with a cotton swab. Cells on the lower surface were fixed with 4% paraformaldehyde and stained with crystal violet. Migrated cells were counted under a light microscope (5 fields/insert) [2]
- Scratch Assay: rASMCs were seeded into 6-well plates and cultured to 100% confluence. A scratch was made in the cell monolayer using a 200 μL pipette tip. Debris was removed by washing with PBS, and medium containing Nicardipine HCl (1-10 μM) was added. Images were taken at 0 and 24 hours. The scratch closure rate was calculated as [(Initial scratch width - Final scratch width) / Initial scratch width] × 100% [2]

Animal/Disease Models: In conscious normotensive rats (NR)[3]
Doses: 0.3-10 mg/kg
Route of Administration: Po
Experimental Results: Induced a dose-dependent hypotensive response (maximal decrease in mean blood pressure, supine position) without any postural hypotensive response.

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1. Antihypertensive Efficacy in SHR:
- Animal Preparation: 12-week-old male SHR (SBP ~180 mmHg) were acclimated for 1 week under standard conditions (12-hour light/dark cycle, 22±1°C, free access to food and water). Mice were randomly divided into 4 groups (n=6/group): control (saline), Nicardipine HCl 0.3 mg/kg, 1 mg/kg, 3 mg/kg [3]
- Drug Formulation and Administration: Nicardipine HCl was dissolved in 0.9% saline (0.5% DMSO as solubilizer) to prepare dosing solutions. For oral administration, drugs were given via gastric gavage (volume: 10 mL/kg). For intravenous administration, drugs were injected via the tail vein (volume: 5 mL/kg) [3]
- Blood Pressure Measurement: SBP and diastolic blood pressure (DBP) were measured using a tail-cuff plethysmograph (pre-warmed to 37°C). For oral studies, measurements were taken before dosing (0 h) and at 0.5, 1, 2, 4, 6, 8 hours post-dosing. For intravenous studies, measurements were taken at 0, 5, 10, 15, 30, 60 minutes post-dosing [3]
2. Cardiac Function Assessment in Anesthetized Dogs:
- Animal Preparation: Male beagle dogs (10-12 kg) were anesthetized with sodium pentobarbital (30 mg/kg, i.v.). A catheter was inserted into the left ventricle via the carotid artery to measure left ventricular pressure (LVP) and calculate dp/dt max (a marker of contractility). A lead II ECG was recorded to monitor heart rate and atrioventricular conduction [3]
- Drug Administration and Data Collection: Nicardipine HCl (0.1 mg/kg, i.v.) was injected slowly over 5 minutes. LVP, dp/dt max, heart rate, and ECG were recorded before dosing and at 5, 15, 30, 60 minutes post-dosing [3]
3. Atherosclerosis Prevention Study in SHR:
- Animal Model: 8-week-old male SHR were fed a high-cholesterol diet (1% cholesterol + 10% lard) for 8 weeks to induce aortic atherosclerosis. Mice were divided into 2 groups (n=6/group): model (high-cholesterol diet + saline) and Nicardipine HCl (high-cholesterol diet + 1 mg/kg/day, p.o.) [3]
- Dosing and Sample Collection: Nicardipine HCl was administered daily via gastric gavage. After 8 weeks, mice were euthanized, and the thoracic aorta was removed. Aortic segments were fixed in 4% paraformaldehyde, embedded in paraffin, and sectioned (5 μm). Sections were stained with hematoxylin-eosin (HE) for wall thickness measurement and Ki-67 antibody for proliferating cell detection [3]

1. Absorption: - Oral bioavailability: In dogs, the absolute bioavailability of nicardipine hydrochloride (2 mg/kg) is approximately 35%, due to significant first-pass metabolism in the liver. In humans, after oral administration of 40 mg nicardipine hydrochloride (immediate-release tablets), the peak plasma concentration (Cmax) is approximately 25 ng/mL, and the time to peak concentration (Tmax) is approximately 1 hour [3]. - Gastrointestinal absorption: Nicardipine hydrochloride is well absorbed in the gastrointestinal tract, with more than 90% of the dose absorbed within 2 hours (as determined by radiolabeled drugs in rats) [3]. 2. Distribution: - Volume of distribution: In rats, the steady-state volume of distribution (Vdss) of nicardipine hydrochloride (1 mg/kg, intravenous injection) is approximately 5 L/kg, indicating its extensive tissue distribution. In dogs, Vdss is approximately 4.2 L/kg [3]
- Tissue concentration: In rats, the highest tissue concentrations are found in the liver (approximately 100 times the plasma concentration) and kidneys (approximately 50 times the plasma concentration). Brain tissue concentrations are less than 5% of plasma concentrations, indicating poor blood-brain barrier penetration [3]
3. Metabolism:
- Major metabolic sites and enzymes: Nicardipine hydrochloride is primarily metabolized in the liver. In humans, CYP3A4 is the major cytochrome P450 enzyme, while CYP2D6 contributes less (<10%) [3]
- Metabolites: The major metabolites are inactive glucuronide conjugates (approximately 70% of total metabolites) and desmethylnicardipine (approximately 10%), the latter being an active metabolite with approximately 10% of the L-VDCC inhibitory activity of the parent drug. No toxic metabolites were found [3]
4. Excretion:
- Routes and rates: In rats, approximately 70% of the radioactive material was excreted in feces (mainly as metabolites) within 72 hours after oral administration of nicardipine hydrochloride (1 mg/kg), and approximately 15% was excreted in urine. In humans, approximately 60% of the dose was excreted in feces within 7 days, and approximately 20% was excreted in urine [3]
5. Elimination:
- Half-life: In dogs, the elimination half-life (t_1/2) of nicardipine hydrochloride (1 mg/kg, intravenous) was approximately 1.5 hours. In humans, the t_1/2 of intravenous administration (0.5 mg/kg) is approximately 2 hours; the half-life of oral administration (40 mg) is approximately 2–3 hours [3]
- Clearance: In rats, the total clearance (CL) is approximately 8 mL/min/kg; in humans, the CL is approximately 6 mL/min/kg [3]
6. Plasma protein binding: Nicardipine hydrochloride has a high plasma protein binding rate: approximately 98% in human plasma, approximately 97% in canine plasma, and approximately 96% in rat plasma (as determined by ultrafiltration) [3]

1. Acute toxicity:
- LD50 value: In mice, the oral LD50 of nicardipine hydrochloride is approximately 1800 mg/kg, and the intravenous LD50 is approximately 30 mg/kg. In rats, the oral LD50 is approximately 2000 mg/kg, and the intravenous LD50 is approximately 25 mg/kg [3]
- Acute symptoms: High-dose intravenous injection (mice >50 mg/kg) can cause hypotension, respiratory depression and arrhythmia (ventricular premature beats) within 10 minutes; death due to circulatory failure within 1 hour [3]
2. Chronic toxicity (6-month study):
- Rats: Daily oral administration of nicardipine hydrochloride (10, 30, 100 mg/kg) caused only a slight increase in liver enzymes (ALT, AST: approximately twice that of the control group) in the 100 mg/kg group; no changes in renal function (BUN, creatinine) or liver and kidney histopathological damage were observed. The above effects were reversible 4 weeks after discontinuation [3] - Dogs: Daily oral administration of nicardipine hydrochloride (5, 15, 50 mg/kg) caused gingival hyperplasia in the 50 mg/kg group (approximately 20% of dogs); no other organ toxicity was observed [3] 3. Drug interactions: - Concomitant use with β-blockers (e.g., propranolol): In dogs, concomitant use enhanced the antihypertensive effect (systolic blood pressure decreased by approximately 15%), but did not cause bradycardia or atrioventricular block [3] - Concomitant use with digoxin: In humans, concomitant use of nicardipine hydrochloride (40 mg, three times daily) with digoxin (0.25 mg/day) did not change the plasma concentrations (Cmax, AUC) of digoxin [3] - Concomitant use with CYP3A4 inhibitors (e.g., ketoconazole): In rats, ketoconazole (10 mg/kg) enhanced the antihypertensive effect (systolic blood pressure decreased by approximately 15%), but did not cause bradycardia or atrioventricular block [3] (mg/kg, intraperitoneal injection) Due to decreased metabolism, the AUC of nicardipine hydrochloride increases by approximately 2.5 times [3]
4. Clinical side effects (reported in human trials):
- Common: headache (approximately 15%), facial flushing (approximately 12%), ankle edema (approximately 8%) [3]
- Uncommon: rash (approximately 2%), transient elevation of liver enzymes (approximately 1%) [3]
- Rare: severe hypotension (<0.5%, seen in patients with volume depletion) [3]

[1]. Electrophysiological analysis of the action of nifedipine and nicardipine on myocardial fibers. Fundam Clin Pharmacol. 1987;1(6):413-31.

[2]. The dihydropyridine calcium antagonist nicardipine reduces aortic smooth muscle cell viability, proliferation and migration. Cardiovascular Research, 2018 Apr,114(1):S43.

[3]. Sherrin H. Baky. Nic ardipine Hydrochloride.

Nicardipine hydrochloride is a dihydropyridine drug with anti-aging effects. Nicardipine hydrochloride is the hydrochloride salt form of nicardipine, a synthetic derivative of nitrophenylpyridine, and a potent calcium channel blocker. Nicardipine (a nifedipine-like drug) blocks calcium ions from entering certain cell walls, inhibiting the contraction of coronary and peripheral arteries, thereby reducing myocardial oxygen consumption and decreasing arterial constriction and spasm. Clinically, it is used as a cerebral and coronary artery vasodilator. (NCI04) It is a potent calcium channel blocker with significant vasodilatory effects. It has antihypertensive effects and can effectively treat angina pectoris and coronary artery spasm without cardiac depressant effects. It is also used to treat asthma and can enhance the effects of certain antitumor drugs. See also: Nicardipine (with active fraction).

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1. Mechanism of action: Nicardipine hydrochloride selectively binds to the α1C subunit (mainly found in vascular smooth muscle) and α1D subunit (found in cardiomyocytes) of L-type voltage-dependent calcium channels (L-VDCCs), blocking the open state of the channels and reducing extracellular Ca2+ influx. This results in: (1) relaxation of vascular smooth muscle (mainly arteries), reducing peripheral vascular resistance and blood pressure; (2) mild inhibition of myocardial Ca2+ influx, resulting in a slight decrease in myocardial contractility, but with no significant effect on heart rate or conduction [1, 3]
2. Therapeutic indications:
- Approved use (1985, Japan; 1988, USA): Treatment of essential hypertension, renovascular hypertension, stable angina and hypertensive emergencies (intravenous preparation) [3]
- Off-label potential: due to its inhibition of vascular smooth muscle proliferation/migration, nicardipine hydrochloride is being investigated for the prevention of restenosis after angioplasty [2]
3. Dosage forms:
- Oral: immediate-release tablets (20 mg, 40 mg; recommended dose: 40 mg, three times daily) and extended-release tablets (80 mg; recommended dose: 80 mg, twice daily) [3]
- Intravenous injection: injection (0.1 mg/mL; Recommended dose: 0.5-6 μg/kg/min, continuous infusion, for hypertensive emergencies) [3]
4. Classification and research and development background: Nicardipine hydrochloride is a second-generation dihydropyridine calcium channel antagonist developed by Yamanouchi Pharmaceutical Co., Ltd. (now Astellas Pharma). It was first approved in Japan in 1985. Its research and development focus is on reducing the cardiac depressive effect of first-generation drugs (such as nifedipine) while maintaining strong antihypertensive activity [3]
5. Comparative advantages: Compared with nifedipine, nicardipine hydrochloride has: (1) a weaker effect on myocardial contractility and action potential duration, thus being safer for patients with heart failure; (2) a longer duration of action, which can reduce the frequency of administration; (3) inhibition of vascular smooth muscle proliferation, which may slow the progression of atherosclerosis [1, 2]

C26H29N3O6.HCL

515.99

515.182

C, 60.52; H, 5.86; Cl, 6.87; N, 8.14; O, 18.60

54527-84-3

Nicardipine-d3 hydrochloride;1432061-50-1;(S)-Nicardipine;76093-36-2;(R)-Nicardipine;76093-35-1;Nicardipine;55985-32-5

41114

Typically exists as light yellow to yellow solids at room temperature

603.4ºC at 760 mmHg

176-1780C

318.7ºC

5.331

2

8

10

36

856

0

O=C(C1=C(C)NC(C)=C(C(OCCN(C)CC2=CC=CC=C2)=O)C1C3=CC=CC([N+]([O-])=O)=C3)OC.[H]Cl

AIKVCUNQWYTVTO-UHFFFAOYSA-N

InChI=1S/C26H29N3O6.ClH/c1-17-22(25(30)34-4)24(20-11-8-12-21(15-20)29(32)33)23(18(2)27-17)26(31)35-14-13-28(3)16-19-9-6-5-7-10-19;/h5-12,15,24,27H,13-14,16H2,1-4H3;1H

2-(Benzylmethylamino)ethyl methyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)pyridine-3,5-dicarboxylatemonohydrochloride

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (4.85 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (4.85 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)