Fig. 1 · Structure

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Nifedipine

Cat. No. A10643 CAS 21829-25-4

L-type calcium channel blocker.

Nifedipine is a L-type calcium channel blocker.

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Biological Activity

Target & Activity

Target Activity Value
calcium channel

Cellular Effect

Cell Line Activity Value Description Reference
A549 IC50 > 100 μM Antiproliferative activity against human A549 cells incubated for 72 hrs by MTT assay [PMID: 31673316]
Calvarial osteoblast EC50 1.54 μM Induction of mineralization in mouse calvarial osteoblasts assessed as increase of mineralized nodules formation after 21 days by alizarin red-S staining based spectrophotometric analysis [PMID: 23214410]
CHO IC50 0.01 μM Inhibition of Cav1.2 current measured using QPatch automatic path clamp system in CHO cells expressing Cav1.2, beta-2 and alpha-2/delta-1 subunits [PMID: 23812503]
CHO IC50 0.05 μM Inhibition of L-type calcium channel measured using 2-electrode voltage-clamp in Chinese hamster ovary cells heterologically expressing alpha-1C subunit [PMID: 22761000]
HCT-116 IC50 > 100 μM Antiproliferative activity against human HCT116 cells incubated for 72 hrs by MTT assay [PMID: 31673316]
HEK293 IC50 0.022 μM Inhibition of L-type calcium channel measured using 2-electrode voltage-clamp in human embryonic kidney cells heterologically expressing alpha-1C subunit [PMID: 22761000]
HEK293 IC50 0.055 μM Inhibition of L-type calcium channel measured using 2-electrode voltage-clamp in human embryonic kidney cells heterologically expressing alpha-1C subunit [PMID: 22761000]
HEK293 IC50 0.086 μM Displacement of [3H]-PN200-110 from voltage-gated calcium channel subunit alpha Cav1.2a (unknown origin) expressed in HEK293 cells after 90 mins by liquid scintillation counting analysis [PMID: 23586669]
HEK-293T IC50 1.5 μM Inhibition of mouse Ido2 transfected in HEK293T cells using L-tryptophan as substrate assessed as kynurenine formation after 45 mins by spectrophotometric analysis [PMID: 23122865]
HEK-293T IC50 46 μM Inhibition of mouse Ido1 transfected in HEK293T cells using L-tryptophan as substrate assessed as kynurenine formation after 45 mins by spectrophotometric analysis [PMID: 23122865]
HepG2 IC50 9.4 μM Cytotoxicity against human HepG2 cells after 24 hrs by LDH release assay [PMID: 30554954]
L929 IC50 6.1 μM Inhibition of human Kv1.5 channel expressed in mouse L929 cells by EP voltage clamp technique [PMID: 19004630]
LLC-MK2 IC50 101.75 μM Antitrypanosomal activity against trypomastigotes of Trypanosoma cruzi infected in rhesus monkey LLC-MK2 cells after 48 hrs by MTT assay [PMID: 20934347]
LLC-MK2 IC50 588.73 μM Cytotoxicity against rhesus monkey LLC-MK2 cells after 48 hrs by MTT assay [PMID: 20934347]
MCF7 IC50 > 100 μM Antiproliferative activity against human MCF7 cells incubated for 72 hrs by MTT assay [PMID: 31673316]
MM1.S IC50 57.9 μM Antiproliferative activity against human MM1S cells incubated for 72 hrs by MTT assay [PMID: 31673316]
SH-SY5Y IC50 1.35 μM Inhibition of human Cav1.3 channel in human SH-SY5Y cells assessed as 70 mM K+ induced calcium elevation compound treated 15 mins before stimulus by Fluo-4/AM assay [PMID: 24754640]
SH-SY5Y IC50 22 μM Inhibition of voltage-dependent L-type calcium channel in 70 mM K+-induced human SH-SY5Y cells assessed as blocking of depolarization-induced Ca2+ uptake by Fluo-4/AM dye based fluorescence microplate reader assay [PMID: 31724859]
Ventricular myocyte IC50 0.05 μM Inhibition of L-type calcium channel measured using whole-cell patch clamp in guinea pig ventricular myocytes [PMID: 22761000]

19 records · Scroll to view more

In Vitro Studies

In GH3/B6/F10 cells after estrogen washout, subsequent E2 or XE addition in the presence of Nifedipine could not elicit calcium influx. In rat pancreatic A-cells under basal conditions, Nifedipine reduced integrated calcium current compared with measurements before addition. In GH3/B6/F10 cells treated with E2 or XE, Nifedipine abolished estrogen-induced PRL secretion in the comparison with and without Nifedipine. [1,2]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Nifedipine and estrogen-stimulated calcium influx

Cell-based study · GH3/B6/F10 cells [1]

In GH3/B6/F10 cells, Nifedipine was added after estrogen washout. Subsequent E2 or XE addition in the presence of Nifedipine could not elicit calcium influx, compared with the E2- or XE-stimulated value.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
change in fluorescence ratio divided by the basal fluorescence [(R – R0)/R0]Reported result Subsequent addition of 10−8 M E2 or XE, in the presence of nifedipine, could not elicit a Ca2+ influx.[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
After washout of the estrogens; followed by a second addition of E2 or XE (10−8 M) in the presence of 10 μM Nifed
Method
added
Co-treatment
Other interventions in this design: E2 10−8 M; KCl 20 mM. Compound effect isolated by the comparison: E2- or XE-stimulated value.
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Nifedipine

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and Methods > Ca2+ measurements. (S11, S20, S21); Results > XE-induced Ca2+ influx is mediated by L-type Ca2+ channels. (S69, S70, S71); Figure 7 legend (S103, S104, S105); Figure 10 legend (S113)

change in fluorescence ratio divided by the basal fluorescence [(R – R0)/R0]: change in fluorescence ratio divided by the basal fluorescence [(R – R0)/R0]; comparator: E2- or XE-stimulated value — Results > XE-induced Ca2+ influx is mediated by L-type Ca2+ channels. (S71); Figure 7 legend (S105)

Nifedipine reduces integrated calcium current in rat pancreatic A-cells

Cell-based study · rat pancreatic A-cells [2]

Rat pancreatic A-cells received Nifedipine under basal conditions. Integrated calcium current decreased compared with measurements before addition.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
integrated Ca2+ currentintegrated Ca2+ current Under basal conditions; 5 μM: 21 ± 2%[2]

Literature-Reported Treatment Conditions

Treatment concentration
5 μM
Exposure duration
the interval between the depolarizations was 2 min
Co-treatment
Other interventions in this design: membrane depolarizations −70 to 0 mV. Compound effect isolated by the comparison: before and after addition.
Reported limits
Not stated in the sentences used: route, vehicle.
Methods and source locations

Compound reported in the paper: Nifedipine

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

materials and methods > Electrophysiology (S12, S19); materials and methods > Solutions (S20); results > Differential Dependence of Exocytosis on Ca2+ Influx through ω-Conotoxin-GVIA– and Nifedipine-sensitive Ca2+ Channels under Basal Conditions and after Activation of PKA (S115); Figure 1 legend (S122); Figure 8 legend (S170, S171, S172)

integrated Ca2+ current: integrated Ca2+ current; comparator: before and after addition — results > Differential Dependence of Exocytosis on Ca2+ Influx through ω-Conotoxin-GVIA– and Nifedipine-sensitive Ca2+ Channels under Basal Conditions and after Activation of PKA (S115); Figure 8 legend (S170)

Nifedipine and estrogen-induced PRL secretion

Cell-based study · GH3/B6/F10 cells; E2/Nifed (n = 32 samples/8 experiments) [1]

GH3/B6/F10 cells were treated with E2 or XE with and without Nifedipine. Nifedipine abolished E2- and XE-induced PRL secretion compared with the E2- or XE-treated value.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
percentage of the basal PRL secretion at each individual time point, normalized to the cell number [crystal violet (CV) signal]Reported result GH3/B6/F10 cells treated with E2 or XE at 10−8 M with 10 μM Nifed: abolished the E2- and XE-induced PRL secretion at 3 min.[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
3 min
Method
new DMEM/0.1% BSA with or without the appropriate reagent or vehicle control (ethanol) was added
Vehicle
ethanol
Co-treatment
Other interventions in this design: E2 10−8 M. Compound effect isolated by the comparison: with and without nifedipine.
Methods and source locations

Compound reported in the paper: Nifedipine

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and Methods > PRL release and radioimmunoassay. (S24); Materials and Methods > Crystal violet assay. (S34); Results > PRL secretion is blocked by nifedipine. (S82, S83); Figure 10 legend (S113, S114, S115, S116)

percentage of the basal PRL secretion at each individual time point, normalized to the cell number [crystal violet (CV) signal]: percentage of the basal PRL secretion at each individual time point, normalized to the cell number [crystal violet (CV) signal]; comparator: E2- or XE-treated value — Results > PRL secretion is blocked by nifedipine. (S83); Figure 10 legend (S113, S115)

In Vivo Studies

Zebrafish embryos received chemical treatment with Nifedipine, and vessel diameter was assessed. Blocking flow led to decreased vessel diameter. [3]

Vessel diameter following flow blockade in zebrafish embryos

Animal study · zebrafish embryos [3]

Zebrafish embryos received chemical treatment with Nifedipine. Blocking flow led to decreased vessel diameter.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
vessel diameterReported result Blocking flow led to a decreased vessel diameter[3]

Conditions shared by the study groups

Route
Chemical treatment
Treatment course
4 hr prior imaging
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Nifedipine 40 μM—Blocking flow led to a decreased vessel diameter[3]
Nifedipine 40 μM
Model: zebrafish embryos
Reported limits: Not stated in the sentences used: vehicle, control.
Methods and source locations

Compound reported in the paper: Nifedipine

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > VEGFR3 controls blood vessels diameter in zebrafish, in a VEGF-C-independent manner (S46, S53, S54); Materials and methods > Zebrafish (S111)

vessel diameter: vessel diameter — Results > VEGFR3 controls blood vessels diameter in zebrafish, in a VEGF-C-independent manner (S54)

Nifedipine 40 μM · Results > VEGFR3 controls blood vessels diameter in zebrafish, in a VEGF-C-independent manner (S53, S54); Materials and methods > Zebrafish (S111)

Specifications

Manufacturer Adooq Bioscience
Actions Blocker
CAS Number 21829-25-4
Applications L-type calcium channel blocker.
Formula C17H18N2O6
Molecular Weight 346.34
SMILES
CC1=C(C(C(=C(N1)C)C(=O)OC)C2=CC=CC=C2[N+](=O)[O-])C(=O)OC

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 66 mg/mL (190.57 mM)
Water Insoluble
Ethanol 14 mg/mL (40.42 mM)

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Wozniak AL, Bulayeva NN, Watson CS. Xenoestrogens at picomolar to nanomolar concentrations trigger membrane estrogen receptor-alpha-mediated Ca2+ fluxes and prolactin release in GH3/B6 pituitary tumor cells. Environ Health Perspect (2005). PMID: 15811834 DOI: 10.1289/ehp.7505 Source material
  2. [2] Gromada J, Bokvist K, Ding WG, et al. Adrenaline stimulates glucagon secretion in pancreatic A-cells by increasing the Ca2+ current and the number of granules close to the L-type Ca2+ channels. J Gen Physiol (1997). PMID: 9276750 DOI: 10.1085/jgp.110.3.217 Source material
  3. [3] Baeyens N, Nicoli S, Coon BG, et al. Vascular remodeling is governed by a VEGFR3-dependent fluid shear stress set point. Elife (2015). PMID: 25643397 DOI: 10.7554/eLife.04645 Source material

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