Cat. No.: HY-P0090

Calcitonin (salmon)

Name: Calcitonin (salmon)
Brand: MedChemExpress
SKU: HY-P0090
Price: 120.00 USD
Availability: InStock
Rating: 5 (3 reviews)

(Synonyms: Salmon calcitonin)

3 Cited Publications

고객리뷰

Based on 3 publication(s) in Google Scholar

Calcitonin (salmon) (Salmon calcitonin) is a calcitonin receptor agonist and osteoclast inhibitor. Calcitonin (salmon) activates the calcitonin receptor/Cyclic AMP (cAMP) (HY-B1511) signaling pathway, binds to the amylin receptor (rat K_d = 30 pmol/L), inhibits osteoclast motility and bone resorption, and lowers plasma calcium. Calcitonin (salmon) induces proteoglycan and type II collagen synthesis, activates skeletal muscle glycogen phosphorylase and adenylate cyclase, stimulates glycogenolysis and increases plasma lactic acid (Lactic acid) (HY-B2227)/glucose (D-Glucose) (HY-B0389), inhibits insulin and gastric acid secretion and gastric emptying, and stimulates renin secretion. Calcitonin (salmon) relieves bone pain and produces antidepressant-like effects by inhibiting hippocampal p38 MAPK/JNK. Calcitonin (salmon) can be used in research on osteoporosis, osteoarthritis, Paget's disease, glucocorticoid-induced osteopenia, hyperglycemia, and depression.

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Purity : 99.96%
CAS No.: 47931-85-1
화학식: C₁₄₅H₂₄₀N₄₄O₄₈S₂
분자량:3431.85

보관:

Sealed storage, away from moisture.

Powder -80°C, 2 years , -20°C, 1 year

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Calcitonin (salmon) Chemical Structure

CAS No.: 47931-85-1

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- 제품 설명
- IC₅₀ & Target
- In Vitro
- In Vivo
Chemical Information
Publications (3)
용액&용해도
- In Vitro
- In Vivo
순도&문서
References
Help & FAQs
Classifications
Bioz

Biological Activity

제품 설명

IC₅₀ & Target

^[6]

p38 MAPK

JNK

All p38 MAPK Isoforms :

All JNK Isoforms :

In Vitro

Carbohydrate MetabolismOxidative StressOthers

Carbohydrate Metabolism

Calcitonin (salmon) (Salmon calcitonin) (10 pM-1 μM; preincubation 30 min-incubation 60 min) inhibits insulin-stimulated glycogen labeling and depletes total glycogen in isolated rat soleus muscle, with an EC₅₀ of 0.4 nM^[5].
Calcitonin (salmon) (10 pM-1 μM; preincubation for 30 min-incubation for 10 min) activates glycogen phosphorylase a in isolated rat soleus muscle strips with an EC₅₀ of 1.4 nM^[5].

Oxidative Stress

Calcitonin (salmon) (7.0 mg/mL; 2-6 h) undergoes PAM-mediated amidation, followed by CEX#3/RP#2 purification of UGL703-derived sCTgly, yielding 85 mg of salmon calcitonin acetate per 1.0 L with a CEX-HPLC purity of 100%^[2].

Others

Calcitonin (salmon) (1 mg/mL; 15 min) is encapsulated in the tested polymeric nanoparticles with an efficiency of 69-83% as determined by indirect RP-HPLC, being highest in PLGA H nanoparticles at 83%^[1].
Calcitonin (salmon) (4 µg/mL; 24 h-42 days) is significantly more stable in 5% acetic acid (HY-Y0319), with 59% remaining at 42 days, whereas in PBS at pH 7.4, 80% degrades within 3 days at 37°C^[1].
Calcitonin (salmon) (100 µg/mL; 24 h) shows almost no adsorption to blank PLGA H/RS or Eudragit RS nanoparticles, with 98-100% remaining at 24 h, and only slight loss to blank PLGA H nanoparticles, with 89.7-94.5% remaining at 24 h^[1].
Calcitonin (salmon) (50 mg; 3-4 weeks) releases very slowly and incompletely from PLGA H and PLGA S nanoparticles, with cumulative release of approximately 21% within 3-4 weeks, whereas Eudragit RS and PLGA/Eudragit RS blends release 80-100% within a few hours^[1].
Calcitonin (salmon) (100 pM-100 nM; 16 days) induces proteoglycan synthesis in human articular cartilage explants, with 10 nM producing 96% of the maximum induction effect^[4].
Calcitonin (salmon) (100 pM-100 nM; 16 days) increases type II collagen formation in human articular cartilage explants, and 10 nM and 100 nM stimulate PIINP release, with a 35% increase over the 100 pM-100 nM range^[4].
Calcitonin (salmon) (1 pM-100 nM; 15 min) activates cAMP signaling in isolated human articular chondrocytes, with maximal induction of > 200% at 1 nM, and the response at 100 nM is reduced by 50% by the calcitonin receptor antagonist 8-32sCT^[4].
Calcitonin (salmon) (100 pM-100 nM; 16 days) does not reduce AlamarBlue metabolic activity in human articular cartilage explants^[4].
Calcitonin (salmon) binds with high affinity (approximately 30 pM) to amylin binding sites in rat brain membranes^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Carbohydrate MetabolismCardiovascular RegulationGlutamate Release or ReceptorsOthers

Carbohydrate Metabolism

Calcitonin (salmon) (100 µg; intravenous injection; single administration) produces greater blood glucose recovery than glucagon (Glucagon (1-29), bovine, human) (HY-P0082) in insulin-induced hypoglycemia and acts synergistically with glucagon^[5].
Calcitonin (salmon) (70 pmol/kg/min (5.5 µg/h); intravenous infusion; continuous; 60 minutes before and 60 minutes after glucose challenge) inhibits the early insulin response to intravenous glucose while elevating plasma glucose^[5].

Carbohydrate Metabolism

Cardiovascular Regulation

Calcitonin (salmon) (Salmon calcitonin) (100 µg; intravenous injection; single administration) acutely elevates plasma lactic acid (Lactic acid) (HY-B2227) in fasted anesthetized rats, subsequently elevates plasma glucose, and does not reduce arterial pressure^[5].
Calcitonin (salmon) (0.01-100 µg; intravenous bolus) produces dose-dependent hyperglycemia with an ED₅₀ of 4.4 µg and no measurable hypotensive effect^[5].

Glutamate Release or Receptors

Calcitonin (salmon) (50 IU/kg; subcutaneous injection; once daily; for 10 consecutive days) attenuates depression-like behavior in CRS-treated mice, accompanied by inhibition of hippocampal p38/JNK phosphorylation, with no change in locomotor activity^[6].

Others

Calcitonin (salmon) (50 IU/kg; subcutaneous injection; once daily; for 10 consecutive days) produces no antidepressant-like behavioral changes in healthy non-stressed mice^[6].
Calcitonin (salmon) (50 IU/kg; subcutaneous injection; once daily; for 10 consecutive days) exhibits antidepressant-like effects in CRS mice, and this effect is blocked by p38 agonism but not by JNK agonism in the FST and SPT^[6].
Calcitonin (salmon) (0.5-6.0 IU/kg; subcutaneous injection; single administration) produces dose-related reductions in serum calcium from 0.5 to 4.0 IU/kg in healthy male Swiss rats, with no further increase at 6.0 IU/kg^[7].
Calcitonin (salmon) (1.0-12.0 IU/kg; intratracheal; single instillation) produces higher relative pulmonary bioactivity in combination with absorption enhancers, reaching 139.1% with the four-component combination F#15 in healthy male Swiss rats^[7].
Calcitonin (salmon) (0.1-0.8 µg/rat; intracerebroventricular injection; single acute) produces a dose-dependent head-twitch response in healthy rats and enhances L-5-Hydroxytryptophan (L-5-HTP) (HY-B1716)-induced head twitches^[8].
Calcitonin (salmon) (20 µg/kg; subcutaneous injection; single acute) alone does not produce head twitches in healthy rats, but enhances L-5-HTP-induced head twitches^[8].
Calcitonin (salmon) (10 U/kg; subcutaneous injection; 5 times per week, Monday to Friday; 4 or 8 weeks) reverses established glucocorticoid-induced osteopenia in rats by enhancing bone formation and inhibiting bone resorption, despite continued MPA use^[9].
Calcitonin (salmon) (2.5-40 U/kg; subcutaneous injection; single injection) produces persistent hypocalcemia and a dose-dependent increase in endogenous serum PTH in rats^[9].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

Harlan-Sprague-Dawley (male; age 95 days; weight 363 g)^[5]
Dosage:

100 µg
Administration:

i.v. bolus; single
Result:

A 100-µg i.v. bolus caused a rapid increase in plasma lactate followed by a slower increase in plasma glucose.
At this dose, efficacy was greatest among the peptides tested.
The same dose did not decrease arterial pressure.

Animal Model:

Harlan-Sprague-Dawley (male)^[5]
Dosage:

0.01, 0.1, 1, 10, 100, 1000 µg
Administration:

i.v. bolus; dose-response series
Result:

The ED₅₀ for the hyperglycemic effect was 4.4 µg.
The ED₅₀ for the plasma lactate increase was not determinable because no clear maximal plateau was defined.
At i.v. doses greater than 1 µg, the effect was greater than that of amylin in elevating plasma lactate.
No significant effect on arterial pressure occurred at any administered dose.

Animal Model:

Harlan-Sprague-Dawley (male; age 72 days; weight 340 g)^[5]
Dosage:

100 µg (single); 100 µg plus glucagon 100 µg (combination)
Administration:

i.v. bolus; single; co-administered with glucagon 100 µg
Result:

After insulin infusion, plasma glucose was 3.2 mmol/L.
A 100-µg bolus produced glycemic recovery of 7.06 mmol/L·h, measured as incremental plasma glucose AUC over 2 h, greater than the recovery with glucagon 100 µg (3.90 mmol/L·h).
Co-administration of 100 µg plus glucagon 100 µg produced a synergistic glycemic recovery of 13.9 mmol/L·h.
Plasma lactate increased.

Animal Model:

Harlan-Sprague-Dawley (male; age 86 days; weight 381 g)^[5]
Dosage:

70 pmol/kg/min (5.5 µg/h)
Administration:

i.v. infusion; continuous; 60 min before and 60 min after glucose challenge
Result:

Continuous infusion elevated plasma glucose relative to controls at various time points throughout the test.
The insulin response within the first 60 min after glucose challenge was 302 pmol/L·h.
During the second hour, insulin levels were higher in infused rats than in controls.

Animal Model:

C57BL/6J (male)^[6]
Dosage:

50 IU/kg bodyweight
Administration:

s.c.; once daily; 10 consecutive days during the 14-day CRS period
Result:

In CRS-treated mice, immobility time in the FST and TST was reduced and sucrose preference in the SPT was increased compared with CRS+saline mice; distance traveled in the OFT was unchanged.
In the hippocampus, phosphorylation ratios of JNK and p38 (p-JNK/JNK and p-p38/p38) were reduced toward control levels, while p-ERK/ERK, p-PTEN/PTEN, p-PI3K/PI3K, p-AKT/AKT, p-mTOR/mTOR, BDNF, PSD95, synapsin-1, and snap25 were unchanged.

Animal Model:

C57BL/6J (male)^[6]
Dosage:

50 IU/kg body weight
Administration:

s.c.; once daily; 10 consecutive days
Result:

Distance traveled in the OFT, immobility time in the FST or TST, and sucrose preference in the SPT were not altered in non-stressed control mice.

Animal Model:

C57BL/6J (male)^[6]
Dosage:

50 IU/kg body weight (sCT); 0.1 mg/kg (AN); 0.2 mg/kg (PMA)
Administration:

s.c. (sCT); once daily; 10 consecutive days; i.p. (AN, PMA); once daily; 15 consecutive days
Result:

In CRS-treated mice, co-application with AN or PMA did not affect locomotor activity in the OFT.
In the TST, immobility time was prolonged by both AN and PMA compared with the saline group under the same stress and dosing conditions.
In the FST and SPT, PMA, but not AN, blocked the antidepressant-like effects.

Animal Model:

Swiss (male albino, 200-220 g)^[7]
Dosage:

0.5, 1.0, 3.0, 4.0, and 6.0 IU/kg
Administration:

subcutaneous; single dose
Result:

At 0.5 IU/kg, mean PBCR was 15.1%; PBCR_max was 25.8%; T.PBCR_max was 90 min; AUC0-240 min was 3543 %·min.
At 1.0 IU/kg, mean PBCR was 20.6%; PBCR_max was 31.2%; T.PBCR_max was 90 min; AUC_0-240 min was 4769 %·min.
At 3.0 IU/kg, mean PBCR was 33.2%; PBCR^max was 46.7%; T.PBCR^max was 150 min; AUC_0-240 min was 7634 %·min.
At 4.0 IU/kg, mean PBCR was 39.3%; PBCR_max was 48.8%; T.PBCR_max was 150 min; AUC_0-240 min was 8885 %·min.
At 6.0 IU/kg, mean PBCR was 39.6%; PBCR_max was 48.9%; T.PBCR_max was 150 min; AUC_0-240 min was 8895 %·min.

Animal Model:

Sprague Dawley (male, 250-300 g)^[8]
Dosage:

0.1, 0.2, 0.4, and 0.8 µg/rat (head-twitch assay); 0.1 µg/rat (L-5-HTP interaction)
Administration:

i.c.v.; single acute doses; 60 min (head-twitch assay); i.c.v.; once; 30 min before carbidopa (interaction)
Result:

Produced a dose-dependent increase in head twitches counted for 60 min at 0.1 µg/rat (n=12), 0.2 µg/rat (n=8), 0.4 µg/rat (n=8), and 0.8 µg/rat (n=8).
In the L-5-HTP interaction study, produced 30.5 head twitches/90 min with 0 mg/kg L-5-HTP (n=12), 50.0 with 12.5 mg/kg L-5-HTP (n=8), 111.4 with 25 mg/kg L-5-HTP (n=7), and 109.0 with 50 mg/kg L-5-HTP (n=6).
Potentiated the head-twitch response elicited by L-5-HTP.

Animal Model:

Sprague Dawley (male, 250-300 g)^[8]
Dosage:

5, 10, 20, 40, and 80 µg/kg (head-twitch assay); 20 µg/kg (L-5-HTP interaction)
Administration:

s.c.; single acute doses; 60 min (head-twitch assay); s.c.; once; 30 min before carbidopa (interaction)
Result:

At 5, 10, 20, 40, and 80 µg/kg, did not change the rat head-twitch response at any tested dose.
In the L-5-HTP interaction study, produced 25.3 head twitches/90 min with 0 mg/kg L-5-HTP (n=8), 17.3 with 12.5 mg/kg L-5-HTP (n=8), 66.0 with 25 mg/kg L-5-HTP (n=8), 104.4 with 50 mg/kg L-5-HTP (n=8), and 187.9 with 100 mg/kg L-5-HTP (n=8).
Potentiated the head-twitch response elicited by L-5-HTP.

Animal Model:

Wistar (female, 11 weeks old at acclimation and 12 weeks old at study start)^[9]
Dosage:

10 U/kg
Administration:

s.c.; 5 times/week Monday-Friday; 4 or 8 weeks
Result:

Restored osteoid and fluorochrome labeling on cancellous bone surfaces, corrected MPA-induced cancellous osteopenia within 4 weeks, and maintained restored bone through 8 weeks.
Histomorphometry showed increased bone formation (OS/BS) and decreased bone resorption parameters (ES/BS and N.Oc).
MPA-induced suppression of serum osteocalcin was reversed at 4 weeks.
Total alkaline phosphatase activity was unchanged.

Animal Model:

Wistar (female, 11 weeks old after 1 week acclimation)^[9]
Dosage:

2.5, 10, and 40 U/kg
Administration:

s.c.; single injection
Result:

Produced long-lasting hypocalcemia and increased serum PTH in a dose-dependent manner over the 1, 3, and 6 h post-injection sampling period.

Related Protocols :

Chemical Information

CAS No. 47931-85-1
Appearance Solid
분자량 3431.85
화학식 C₁₄₅H₂₄₀N₄₄O₄₈S₂
Color White to off-white
Synonyms

Salmon calcitonin
Sequence

Cys-Ser-Asn-Leu-Ser-Thr-Cys-Val-Leu-Gly-Lys-Leu-Ser-Gln-Glu-Leu-His-Lys-Leu-Gln-Thr-Tyr-Pro-Arg-Thr-Asn-Thr-Gly-Ser-Gly-Thr-Pro-NH2 (Disulfide bridge: Cys1-Cys7)
Sequence Shortening

CSNLSTCVLGKLSQELHKLQTYPRTNTGSGTP-NH2 (Disulfide bridge: Cys1-Cys7)
선적

Room temperature in continental US; may vary elsewhere.

보관

Sealed storage, away from moisture

Powder	-80°C	2 years
	-20°C	1 year

* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

Publications (3)

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J Cell Mol Med

Calcitonin inhibits intervertebral disc degeneration by regulating protein kinase C. [Abstract]

2020 Aug;24(15):8650-8661. PMID: 32564456

Calcitonin (salmon) purchased from MedChemExpress. Usage Cited in: J Cell Mol Med. 2020 Aug;24(15):8650-8661. [Abstract]

Calcitonin increases phosphorylated PKC-ε but reduces phosphorylated PKC-δ, which are antagonistic to the effects of IL-1 treatment.
bioRxiv

2026 Jun 19.
bioRxiv

2025 Nov 21.

용액&용해도

In Vitro:

H₂O : 50 mg/mL (14.57 mM; Need ultrasonic)

DMSO : 50 mg/mL (14.57 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

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Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

0.2914 mL

1.4569 mL

2.9139 mL

5 mM

0.0583 mL

0.2914 mL

0.5828 mL

10 mM

0.0291 mL

0.1457 mL

0.2914 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

몰농도 계산기

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

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Volume Volume

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Volume _(start) Volume _(start)

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Volume _(final) Volume _(final)

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (0.73 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (0.73 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (0.73 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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g
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Working solution concentration: 0.22 mg/mL

This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact

MedChemExpress (MCE) .

순도&문서

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

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References

[1]. Glowka E, et al. Preparation and in vitro-in vivo evaluation of salmon calcitonin-loaded polymeric nanoparticles. Journal of microencapsulation. 2010;27(1):25-36.

[2]. Ray MV, et al. Production of salmon calcitonin by direct expression of a glycine-extended precursor in Escherichia coli. Protein expression and purification. 2002 Nov;26(2):249-59.

[3]. Trier S, et al. Acylation of salmon calcitonin modulates in vitro intestinal peptide flux through membrane permeability enhancement. European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V. 2015 Oct;96:329-37.

[4]. Sondergaard BC, et al. Investigation of the direct effects of salmon calcitonin on human osteoarthritic chondrocytes. BMC musculoskeletal disorders. 2010 Apr 05;11:62.

[5]. Young AA, et al. Diabetogenic effects of salmon calcitonin are attributable to amylin-like activity. Metabolism: clinical and experimental. 1995 Dec;44(12):1581-9.

[6]. Zhu W, et al. (2023) Chronic salmon calcitonin exerts an antidepressant effect via modulating the p38 MAPK signaling pathway. Front. Mol. Neurosci. 16:1071327.

[7]. Mahesh Kumar T, et al. Pulmonary absorption enhancement of salmon calcitonin. Journal of drug targeting. 2004 Apr;12(3):135-44.

[8]. Gaggi R, et al. Salmon calcitonin induced head twitch in the rat. Japanese journal of pharmacology. 1988 May;47(1):87-90.

[9]. Furuichi H, et al. Bone-anabolic effect of salmon calcitonin on glucocorticoid-induced osteopenia in rats. Biological & pharmaceutical bulletin. 2000 Aug;23(8):946-51.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
H₂O / DMSO	1 mM	0.2914 mL	1.4569 mL	2.9139 mL	7.2847 mL
	5 mM	0.0583 mL	0.2914 mL	0.5828 mL	1.4569 mL
	10 mM	0.0291 mL	0.1457 mL	0.2914 mL	0.7285 mL

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

Bioz

Calcitonin (salmon)

3 Cited Publications

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Calcitonin (salmon)

Publications Citing Use of MedChemExpress (MCE) Calcitonin (salmon)

All p38 MAPK Isoforms

All JNK Isoforms