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Calcium chloride anhydrous, for cell culture (Calcium dichloride anhydrous, for cell culture)

Calcium chloride anhydrous, for cell culture (Calcium dichloride anhydrous, for cell culture)
Calcium chloride anhydrous, for cell culture (Calcium dichloride anhydrous, for cell culture) Chemical Structure CAS No.: 10043-52-4
Product category: Biochemical Assay Reagents
This product is for research use only, not for human use. We do not sell to patients.
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Product Description
Calcium chloride anhydrous, for cell culture is an inorganic salt that can be used in the preparation of various buffers.
Biological Activity I Assay Protocols (From Reference)
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Approximately 80% of calcium in the body is excreted in the form of insoluble salts via feces; the remaining 20% is excreted in urine. Rat placentas were double-perfused in vivo using a modified Kjeldahl solution. Perfusion was performed via the femoral artery on the maternal side and the umbilical artery on the fetal side. Transport of 45Ca2+ and 3(H)L-glucose in the placenta was measured in the maternal-fetal direction. The transcellular component Jmf,tc of maternal-fetal Ca2+ transport was estimated based on the transport rates of the two tracers and the Ca2+ concentration [Ca2+]m in the maternal perfusion fluid. When [Ca2+]m was 11 mM (the physiological concentration of Ca2+ in plasma), Jmf,tc was 92.4 ± 13.7 nM min⁻¹ (mean ± standard deviation), approximately 90% of the expected transport volume in the intact placenta. The placental permeability-surface area product (PS) to 3(H)L-glucose was 13.8 ± 3.9 μL min⁻¹, approximately four times the expected value for an intact placenta. The transport of 45Ca²⁺ changed rapidly with variations in [Ca²⁺]m. The kinetic constants for Ca²⁺ transcellular transport were the Michaelis constant Km = 0.45 mM and the maximum transport rate Vmax = 116 nM min⁻¹. This indicates that, at physiological Ca²⁺ levels, Ca²⁺ transport to the fetus is relatively independent of changes in [Ca²⁺]m. Strontium and barium (SrCl₂ and BaCl₂, 1 mM) reduced Jmf,tc; this reaction was rapid and reversible. Magnesium (2 mM) had no such effect. Increasing [Ca²⁺]m from 0.35 mM to 2 mM rapidly and reversibly reduced the translocation of 85Sr²⁺ and 133Ba²⁺ between the mother and fetus. These observations indicate that Sr²⁺ and Ba²⁺ are transported across the placenta via the Ca²⁺ transport system. This implies that the transport is not substrate-specific. Cadmium (1 mM-CdCl₂) irreversibly reduced Jmf,tc with a certain latency. The slowness of this response suggests the presence of non-competitive inhibition. Cadmium (0.02 mM-CdCl₂) had no effect on Jmf,tc. 7. Maternal administration of the calcium channel blocker nifedipine (10 μM) had no effect on Jmf,tc. /Calcium Salts/
The paracellular and transcellular pathway components of calcium ion transport in perfused human placental chorionic membranes were dissected, and the nature of the transcellular pathway components was investigated. The transport of 45Ca²⁺ and chromium (51)CR-labeled ethylenediaminetetraacetic acid in in vitro perfused human placental chorionic membranes was measured, and the paracellular and transcellular pathway components of calcium ion transport were calculated based on the transport of the two tracers. The transcellular pathway component of maternal-fetal calcium ion transport accounts for approximately one-third of total maternal-fetal transport. This component is sensitive to cyanide but insensitive to verapamil and exhibits saturation. The fetal-maternal transcellular pathway component did not differ significantly from zero. The in vitro transport rate correlated well with the in vivo transport rate estimated from reported data. Ca²⁺ undergoes significant maternal-fetal active transport across the human placenta. /Calcium Salts/
Metabolism/Metabolites
Approximately 80% of calcium in the body is excreted in the form of insoluble salts in feces; the remaining 20% is excreted in urine.
Toxicity/Toxicokinetics
Interactions
In the early growth stages of sesame variety PB-1, the decrease in fresh and dry weight under 1.0 mM Cd²⁺ treatment was greater than that under the same concentrations of Pb²⁺ and Cu²⁺ treatment. When 10.0 mM (1.9 EC) calcium chloride and different combinations of metal salts were applied simultaneously to growing seedlings, both root fresh and dry weights were significantly restored. The accumulation of divalent Pb, Cd, and Cu varied depending on the metal species and plant part, with or without the application of 10.0 mM calcium chloride. The order of endogenous metal accumulation was Cu > Cd > Pb, and the amount of metal accumulated in roots was higher than in leaves regardless of the application of calcium chloride. Calcium chloride could restore the nitrogen reduction activity (NRA) loss in roots caused by any metal combination, while salts could only restore the leaf NRA loss caused by lead and cadmium (Pb-Cd, both at 1.0 mM). On the other hand, when enzyme activity was directly measured using in vitro assays, the NRA responses in roots and leaves differed, and salts significantly accelerated the loss of enzyme activity. However, both application of calcium chloride alone and application of calcium chloride in combination with different metals significantly increased the organic nitrogen content in roots and leaves (p < 0.001). Data showed that adding 10.0 mM calcium chloride to the root environment of sesame seedlings significantly reduced the endogenous accumulation of divalent copper, cadmium, and lead in roots and leaves, and greatly alleviated metal toxicity, which is beneficial to the growth of seedling roots and leaves and nitrate reduction. Diltiazem is commonly used to treat atrial fibrillation or flutter (AFF) with rapid ventricular rate (RVR). Although it is very effective in controlling heart rate, it has been reported that the incidence of hypotension (defined as systolic blood pressure (SBP) < 90 mmHg) induced by diltiazem is as high as 18%, with multiple studies (including more than 450 patients) reporting an average incidence of 9.7%. This hypotension may complicate treatment. This study aimed to determine whether calcium chloride (CaCl2) pretreatment could reduce the decrease in systolic blood pressure (SBP) after intravenous diltiazem while maintaining the efficacy of diltiazem. This was a prospective, randomized, double-blind, placebo-controlled study. A total of 78 patients with atrial fibrillation (AFF) and a ventricular rate ≥ 120 bpm were included. Half of the patients received intravenous CaCl2 pretreatment, and the other half received placebo. All patients subsequently received a standard weight-based intravenous dose of diltiazem. If further heart rate control was clinically required, a second CaCl2 pretreatment or placebo combined with diltiazem was administered. The degree of heart rate reduction was comparable between the CaCl2 and placebo pretreatment groups (p < 0.001). No adverse events occurred in the calcium pretreatment group. One patient in the placebo group experienced worsening paradoxical tachycardia and apnea after diltiazem infusion. Although the safety profile of intravenous calcium chloride (CaCl2) as a pretreatment for acute femoral head necrosis (AFF) with rapid venous flow reserve (RVR) appeared comparable to placebo, the researchers failed to find that intravenous calcium chloride pretreatment significantly reduced the decrease in systolic blood pressure (SBP). To investigate the effects of calcium chloride on sodium chloride (NaCl)-induced oxidative stress, researchers cultivated periwinkle (Catharanthus roseus (L.) G. Don.) in both sodium chloride and calcium chloride solutions and measured indicators such as lipid peroxidation (TBARS content), hydrogen peroxide (H2O2) content, osmotic pressure concentration, proline (PRO) metabolic enzyme activity, antioxidant enzyme activity, and indole alkaloid accumulation. Plants were treated individually with 80 mM NaCl solution, 80 mM NaCl + 5 mM CaCl2 solution, and 5 mM CaCl2 solution, respectively. Control plants were irrigated with groundwater. Plants were randomly removed 90 days after sowing (DAS). Compared to the control group, plants under NaCl stress showed increased levels of TBARS, H₂O₂, glycine betaine (GB), and proline (PRO), decreased proline oxidase (PROX) activity, and increased γ-glutamyl kinase (γ-GK) activity. Adding CaCl₂ to plants under NaCl stress reduced PRO concentration by increasing PROX levels and decreasing γ-GK activity. Calcium ions increased GB content. CaCl₂ appeared to enhance osmotic protection by synergistically promoting GB accumulation with NaCl. The activities of antioxidant enzymes superoxide dismutase (SOD), peroxidase (POX), and catalase (CAT) were all increased under salt stress, and CaCl₂ treatment further enhanced these enzyme activities. Compared with plants treated with sodium chloride alone and untreated plants, the total indole alkaloid content in the stems and roots of periwinkle plants treated with both sodium chloride and calcium chloride was increased. This study aimed to evaluate the effects of calcium chloride on hemodynamics in a canine acute propranolol poisoning model. Two minutes after propranolol infusion (10 mg/kg), each dog received one of two treatments: first, an intravenous bolus of 0.125 mL/kg of 10% calcium chloride solution, followed by a continuous infusion of 0.375 mL/kg over the next 30 minutes; second, an intravenous bolus of an equal volume of normal saline, followed by a continuous infusion. Compared to the saline-treated control group, calcium chloride significantly improved the propranolol-induced decrease in cardiac index and stroke volume (overall α=0.05). Furthermore, compared to the saline group, the calcium chloride group showed earlier improvement in propranolol-induced mean arterial pressure, changes in maximum left ventricular pressure over time, and peripheral vascular resistance (overall α=0.05). We observed no difference in propranolol-induced bradycardia or QRS interval prolongation among the treatment groups. In this acute propranolol poisoning model, calcium chloride treatment improved the impaired hemodynamic status, primarily through positive inotropic effects. For more complete data on calcium chloride interactions (16 items in total), please visit the HSDB record page.
Non-human toxicity values
Oral LD50 for male rabbits: 755 mg/kg body weight
Oral LD50 for male rabbits: 507 mg/kg body weight
Dermal LD50 for rabbits: >5000 mg/kg body weight
Intramuscular LD50 for rats: 25 mg/kg body weight
For more complete (22) non-human toxicity values of calcium chloride, please visit the HSDB record page.
References

[1].Facile Tetrahydropyranylation of Alcohols and Phenols Using Anhydrous Calcium Chloride under Mild and Neutral Conditions. Volume 134, pages 425–428, (2003) Cite this article.

Additional Infomation
Calcium chloride is a white to off-white solid, readily soluble in water and sinking to the bottom. (US Coast Guard, 1999)
Calcium dichloride is a calcium salt, belonging to the inorganic chloride and inorganic calcium salts. It can be used as a fertilizer.
Calcium chloride is an ionic compound of calcium and chlorine, extremely soluble in water, and deliquescent. It is a solid salt at room temperature, with properties similar to typical ionic halides. It has many common uses, such as brine for refrigeration equipment, road de-icing and dust removal agents, and cement raw materials. Calcium chloride can be produced directly from limestone, but the Solvay process also produces a large amount of calcium chloride as a byproduct. Due to its hygroscopic nature, it must be stored in sealed containers.
Calcium chloride is a white crystalline substance, readily soluble in water. Calcium chloride is a chloride of calcium, a divalent metallic element that plays many important roles in organisms. Calcium is a major component of bones and also plays a variety of roles as an intracellular ion and plasma ion. In medicine, calcium chloride is often used as a 10% injection to supplement calcium. (NCI04)
Calcium chloride is a salt used to supplement calcium, as an acid-producing diuretic, and as an antidote for magnesium poisoning.
See also: Chloride ions (with active moiety) Calcium cations (containing active moiety)...See more...
Drug Indications
For the treatment of hypocalcemia requiring a rapid increase in plasma calcium levels, for the treatment of magnesium poisoning due to magnesium sulfate overdose, and to counteract the adverse effects of hyperkalemia as measured by electrocardiogram (ECG) up to the correction of elevated potassium levels in the extracellular fluid.
Mechanism of Action
Calcium chloride dissociates upon dissolving in water, releasing calcium ions (Ca²⁺) and chloride ions (Cl⁻). These are normal components of body fluids and depend on various physiological mechanisms to maintain a balance between intake and excretion. In hyperkalemia, the influx of calcium ions helps restore the normal gradient between the threshold potential and the resting membrane potential.
Therapeutic Uses
Therapeutic Category (Veterinary): Can be used to treat hypocalcemia, such as postpartum paralysis.
Therapeutic Category: Electrolyte supplement. Formerly used as a diuretic, urine acidifier, and antihistamine.
/SRP: Calcium gluconate has replaced calcium chloride in many therapeutic indications. / 10% calcium chloride injection (USP) is indicated for: (1) the treatment of hypocalcemia requiring a rapid increase in plasma calcium levels; (2) the treatment of magnesium poisoning due to magnesium sulfate overdose; (3) the elimination of the harmful effects of hyperkalemia as measured by electrocardiogram (ECG) prior to correcting elevated potassium levels in the extracellular fluid. 10% calcium chloride injection (USP) may also be used for cardiac resuscitation, especially when myocardial contractility is weakened or insufficient after defibrillation, or when adrenaline injection fails to enhance myocardial contractility.
/Experimental Treatment: / Between March 3, 1987, and September 8, 1989, we treated 28 patients (38 limbs) with hydrofluoric acid poisoning who had not responded to local treatment with intra-arterial calcium infusion. Although 18 of the injuries occurred in the workplace, only one patient used hydrofluoric acid at a concentration higher than 12%. Many such products are available without a prescription. Most patients did not wear protective equipment and lacked awareness of the risks posed by the product. Symptoms (pain, erythema, and edema) appeared 1 to 6 hours after exposure. After arterial catheter insertion, patients began treatment with a continuous infusion of 10 ml of 10% calcium chloride solution diluted in 40 ml of normal saline over 4 hours. Each patient was given 4–8 hours of rest before assessment for re-infusion. Serum calcium, magnesium, phosphorus, prothrombin time (PT), and partial thromboplastin time (PTT) were monitored. Infusions were repeated until the patient was no longer tender. Compared to previous reports, the number of infusions increased with tenderness as the endpoint. The mean number of infusions was 4.1 (range 1–10). The complete healing rate was 100%. Serum calcium levels were significantly elevated but did not reach dangerous levels (range 9.3–12.8 mmol/L). Simultaneously, serum magnesium levels decreased significantly, even to the point where intravenous magnesium supplementation was required. Phosphorus, PT, and PTT showed no significant changes.
For more complete data on the therapeutic uses of calcium chloride (7 types), please visit the HSDB record page.
Drug Warnings
Calcium chloride should not be administered intramuscularly, subcutaneously, or perivascularly, as severe necrosis and sloughing may occur.
Calcium chloride is contraindicated for cardiac resuscitation in patients with ventricular fibrillation or pre-existing digitalis toxicity.
This product contains potentially toxic aluminum. Prolonged parenteral administration may lead to toxic aluminum levels in patients with impaired renal function. Premature infants are particularly vulnerable because their kidneys are not yet fully developed and they require large amounts of aluminum-containing calcium and phosphate solutions. Studies have shown that in patients with impaired renal function, including premature newborns, aluminum accumulation levels in the body can reach levels associated with central nervous system and bone toxicity if parenteral doses exceed 4 to 5 micrograms/kg/day. Tissue accumulation may occur even at lower doses.
FDA Pregnancy Risk Classification: C / Risk cannot be ruled out. There is a lack of adequate, well-controlled human studies, and animal studies have not shown any risk to the fetus, or data are lacking. There is a possibility of fetal harm if this medication is used during pregnancy; however, the potential benefits may outweigh the potential risks. /
Rapid injection may cause a stinging sensation, a calcium odor, a feeling of pressure, or a "heat wave" in the patient. Injection of calcium chloride may be accompanied by peripheral vasodilation and a local "burning" sensation; a moderate drop in blood pressure may occur. If perivascular infiltration occurs, intravenous administration to that site should be stopped immediately. Local infiltration of the affected area with a 1% procaine hydrochloride solution (with the addition of hyaluronidase) can usually reduce venous spasms and dilute residual calcium in the local tissue. Local heat application may also be helpful.
Pharmacodynamics
Calcium is the fifth most abundant element in the human body, primarily found in bone structure. Calcium plays important physiological roles, but many of its mechanisms are not fully understood. It is essential for the functional integrity of the nervous and muscular systems. Calcium is essential for normal heart function and is also one of the factors that play a role in blood clotting mechanisms.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
CACL2
Molecular Weight
110.98
Exact Mass
109.9
CAS #
10043-52-4
PubChem CID
5284359
Appearance
White cubic crystals or powder
Cubic crystals, granules or fused masses
White .. lumps of flakes
Density
1.086 g/mL at 20 °C
Boiling Point
1600 °C
Melting Point
772 °C(lit.)
Flash Point
>1600°C
Vapour Pressure
0.01 mm Hg ( 20 °C)
Index of Refraction
n20/D 1.358
LogP
1.379
Hydrogen Bond Donor Count
0
Hydrogen Bond Acceptor Count
2
Rotatable Bond Count
0
Heavy Atom Count
3
Complexity
0
Defined Atom Stereocenter Count
0
InChi Key
UXVMQQNJUSDDNG-UHFFFAOYSA-L
InChi Code
InChI=1S/Ca.2ClH/h;2*1H/q+2;;/p-2
Chemical Name
calcium;dichloride
HS Tariff Code
2934.99.9001
Storage

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, avoid exposure to moisture.
Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
Typically soluble in DMSO (e.g. 10 mM)
Solubility (In Vivo)
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

Injection Formulations
(e.g. IP/IV/IM/SC)
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution 50 μL Tween 80 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO 400 μLPEG300 50 μL Tween 80 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).
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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO 100 μLPEG300 200 μL castor oil 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10: 10 : 80 (i.e. 100 μL Ethanol 100 μL Cremophor 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH 400 μLPEG300 50 μL Tween 80 450 μL Saline)


Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).
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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders


Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 9.0106 mL 45.0532 mL 90.1063 mL
5 mM 1.8021 mL 9.0106 mL 18.0213 mL
10 mM 0.9011 mL 4.5053 mL 9.0106 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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In vivo Formulation Calculator (Clear solution)
Step 1: Enter information below (Recommended: An additional animal to make allowance for loss during the experiment)
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Calculation results

Working concentration mg/mL;

Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
             (2) Be sure to add the solvent(s) in order.

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