PamidronateCAS# 40391-99-9 |
- GDC-0068 (RG7440)
Catalog No.:BCC1271
CAS No.:1001264-89-6
- MK-2206 dihydrochloride
Catalog No.:BCC1274
CAS No.:1032350-13-2
- AZD5363
Catalog No.:BCC1073
CAS No.:1143532-39-1
- A-443654
Catalog No.:BCC1321
CAS No.:552325-16-3
- AKT inhibitor VIII
Catalog No.:BCC1334
CAS No.:612847-09-3
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 40391-99-9 | SDF | Download SDF |
PubChem ID | 4674 | Appearance | Powder |
Formula | C3H11NO7P2 | M.Wt | 235.07 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | H2O : 2 mg/mL (8.51 mM; Need ultrasonic) DMSO : < 1 mg/mL (insoluble or slightly soluble) | ||
Chemical Name | (3-amino-1-hydroxy-1-phosphonopropyl)phosphonic acid | ||
SMILES | NCCC(O)([P](O)(O)=O)[P](O)(O)=O | ||
Standard InChIKey | WRUUGTRCQOWXEG-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C3H11NO7P2/c4-2-1-3(5,12(6,7)8)13(9,10)11/h5H,1-2,4H2,(H2,6,7,8)(H2,9,10,11) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
||
About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
||
Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Pamidronic acid is a drug used to treat a broad spectrum of bone absorption diseases.In Vitro:Osteosarcoma cell viability decreases significantly in a concentration- and time-dependent manner at pamidronate concentrations ranging from 100 to 1000 μM, most consistently after 48 and 72 hours' exposure. In treated osteosarcoma cells, the lowest percentage cell viability is 34% (detected after 72 hours' exposure to 1000μM pamidronate)[1]. Pamidronate disodium inhibits Wnt and β-catenin signaling, which controls osteogenic differentiation in BMMSCs. Wnt3a, a Wnt and β-catenin signaling activator, reverses the negative effects caused by pamidronate disodium to salvage the osteogenic defect in BMMSCs[2].In Vivo:Pamidronic acid can significantly inhibit and even reverse early osteoarthritic subchondral bone loss, thus alleviating the process of cartilaginous degeneration. The mechanisms involved may be associated with the upregulation of OPG expression, and downregulation of RANKL, MMP-9 and TLR-4 expression[3]. References: |
Pamidronate Dilution Calculator
Pamidronate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 4.2541 mL | 21.2703 mL | 42.5405 mL | 85.081 mL | 106.3513 mL |
5 mM | 0.8508 mL | 4.2541 mL | 8.5081 mL | 17.0162 mL | 21.2703 mL |
10 mM | 0.4254 mL | 2.127 mL | 4.2541 mL | 8.5081 mL | 10.6351 mL |
50 mM | 0.0851 mL | 0.4254 mL | 0.8508 mL | 1.7016 mL | 2.127 mL |
100 mM | 0.0425 mL | 0.2127 mL | 0.4254 mL | 0.8508 mL | 1.0635 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
Pamidronate
- 6-Methoxykaempferol 3-O-rutinoside
Catalog No.:BCN2379
CAS No.:403861-33-6
- Benzyl 2-hydroxy-6-(beta-glucosyloxy)benzoate
Catalog No.:BCN7434
CAS No.:403857-21-6
- HEMADO
Catalog No.:BCC7118
CAS No.:403842-38-6
- 10058-F4
Catalog No.:BCC1050
CAS No.:403811-55-2
- Qc 1
Catalog No.:BCC6356
CAS No.:403718-45-6
- Cannabisin H
Catalog No.:BCN3896
CAS No.:403647-08-5
- Obtusafuran methyl ether
Catalog No.:BCN8103
CAS No.:40357-59-3
- Isoneobavaisoflavone
Catalog No.:BCN3195
CAS No.:40357-43-5
- p-Menth-1-ene-3,6-diol
Catalog No.:BCN5454
CAS No.:4031-55-4
- Cassyfiline
Catalog No.:BCN4763
CAS No.:4030-51-7
- MDL 12330A hydrochloride
Catalog No.:BCC7066
CAS No.:40297-09-4
- Telaprevir (VX-950)
Catalog No.:BCC2107
CAS No.:402957-28-2
- Capsaicin
Catalog No.:BCN1016
CAS No.:404-86-4
- erythro-1-Phenylpropane-1,2-diol
Catalog No.:BCN6596
CAS No.:40421-52-1
- Pinusolidic acid
Catalog No.:BCN5455
CAS No.:40433-82-7
- Kaempferol-3-O-glucorhamnoside
Catalog No.:BCN2830
CAS No.:40437-72-7
- Yatein
Catalog No.:BCN5456
CAS No.:40456-50-6
- Bursehernin
Catalog No.:BCN3040
CAS No.:40456-51-7
- Ethyl ferulate
Catalog No.:BCN1257
CAS No.:4046-02-0
- Panobinostat (LBH589)
Catalog No.:BCC3601
CAS No.:404950-80-7
- LAQ824 (NVP-LAQ824,Dacinostat)
Catalog No.:BCC2160
CAS No.:404951-53-7
- Z-Lys(Z)-OH
Catalog No.:BCC2762
CAS No.:405-39-0
- 4'-Demethylpodophyllotoxin
Catalog No.:BCN2625
CAS No.:40505-27-9
- Salubrinal
Catalog No.:BCC4843
CAS No.:405060-95-9
The Effect of Locally Administered Pamidronate on Autogenous Bone Graft in Maxillofacial Reconstruction: A Randomized Clinical Trial.[Pubmed:28299027]
Int J Organ Transplant Med. 2017;8(1):43-47. Epub 2017 Feb 1.
BACKGROUND: Although bone grafts are commonly used in reconstructive surgeries, they are sensitive to local perfusion and are thus prone to severe resorption. Biphosphonates can inactivate osteoclasts and can be used to control the undesirable bone resorption. OBJECTIVE: To assess the effect of administration of biphosphonates on bone resorption. METHODS: 20 patients with bony defects who were candidates for free autogenous grafts were randomized into "Pamidronate" and "control" groups. Bone segments were soaked in either Pamidronate solution or normal saline and were inserted into the area of the surgery. Bone densities were measured post-surgery and in 6-month follow-up. Data were obtained via Digora software and analyzed. RESULTS: The mean+/-SD bone density in Pamidronate group changed from 93.4+/-14.6 to 93.6+/-17.5 (p<0.05); in the control group the density decreased from 89.7+/-13.2 to 78.9+/-11.4 (p<0.05). The mean difference of bone density in anterior areas of the jaws showed higher DXA in comparison to posterior regions (p=0.002). CONCLUSION: Locally administered Pamidronate affects reduction in bone resorption.
Preparation and evaluation of rhenium-188-pamidronate as a palliative treatment in bone metastasis.[Pubmed:28279906]
Nucl Med Biol. 2017 Jun;49:1-7.
OBJECTIVE: Rhenium-188-hydroxyethylidene diphosphonate ((188)Re-HEDP) as a first generation bisphosphonate has been widely used for bone seeking radiopharmaceutical in cases of metastatic bone disease. No study has been yet reported on preparing a complex of (188)Re with Pamidronate (3-aminohydroxypropylidene-1,1-bisphosphonic acid) (PMA) as a second generation bisphosphonate. Based on this fact, it was hypothesized that a bone-seeking (188)Re-PMA radiopharmaceutical could be developed as an agent for palliative radiotherapy of bone pain due to skeletal metastases. METHODS: Pamidronate was labeled with (188)ReO4(-) eluted from the alumina based (188)W/(188)Re generator. Labeling was optimized, and radiochemical analysis was performed by thin layer chromatography (TLC) and high performance liquid chromatography (HPLC). Biodistribution of this radioconjugate was evaluated and verified further in mice. RESULTS: (188)Re-PMA was prepared successfully in a high labeling yield (>95%) corresponding to a specific activity of 124MBq/mumol and good in vitro stability, but it is likely to consist of multiple species. In biodistribution studies selective uptake and retention of activity in the skeletal system (0.81+/-0.25% ID/g and 0.57+/-0.16 at 4 and 48h in bone post injection respectively) followed by clearance in the soft tissues were observed. CONCLUSION: These results show that due to its biological capabilities it would be advantageous to use (188)Re-PMA for bone pain palliation therapy.
Pamidronate Attenuates Oxidative Stress and Energetic Metabolism Changes but Worsens Functional Outcomes in Acute Doxorubicin-Induced Cardiotoxicity in Rats.[Pubmed:27889760]
Cell Physiol Biochem. 2016;40(3-4):431-442.
BACKGROUND: Cardiotoxicity is the major side effect of doxorubicin. As mechanisms that are involved in cardiotoxicity are ambiguous, new methods for attenuating cardiotoxicity are needed. Recent studies have shown that bisphosphonates can decrease oxidative stress. Therefore, the objective of this study was to evaluate the effect of Pamidronate on preventing acute doxorubicin-induced cardiotoxicity. METHODS: Sixty-four male Wistar rats were allocated into four groups: the control group (C), the Pamidronate group (P), the doxorubicin group (D) and the doxorubicin/Pamidronate group (DP). The rats in the P and DP groups received Pamidronate injections (3 mg/kg, IP). After 24 hours, the rats in the D and DP groups received doxorubicin injections (20 mg/kg, IP). Forty-eight hours after doxorubicin injection, the rats were killed. Echocardiography, isolated heart study and biochemical analysis were performed. RESULTS: Doxorubicin-induced acute cardiotoxicity showed increased matrix metalloproteinases (MMP)-2 activation, oxidative damage and induced alterations in myocardial energetic metabolism. Pamidronate did not inhibit MMP-2 activation but attenuated oxidative stress and improved myocardial energetic metabolism. Regarding cardiac function, the DP group exhibited a decrease in the left ventricular ejection fraction in the echocardiography and a decrease in +dP/dt in the isolated heart study compared with other groups. The same DP group presented serum hypocalcaemia. CONCLUSIONS: Despite its ability to reduce oxidative stress and improve energy metabolism in the heart, Pamidronate worsened systolic function in rats treated with doxorubicin, and therefore we cannot recommend its use in conjunction with anthracycline chemotherapy.