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Статті в журналах з теми "Gallium nitrate"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Hughes, Thomas E., and Lea Ann Hansen. "Gallium Nitrate." Annals of Pharmacotherapy 26, no. 3 (March 1992): 354–62. http://dx.doi.org/10.1177/106002809202600310.

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OBJECTIVE: To evaluate the therapeutic role of gallium nitrate in the treatment of hypercalcemia associated with malignancy and related disease states. DATA SOURCES: A literature search of English-language studies involving gallium nitrate for the period 1966–1991 using MEDLINE and the bibliographies of relevant articles. STUDY SELECTION: Because of the limited number of studies, all clinical trials were reviewed, with particular emphasis on Phase III comparative trials. Related investigative studies on the pharmacology, pharmacokinetics, and toxicity of gallium nitrate were also reviewed. DATA EXTRACTION: Two appraisers independently abstracted data from available clinical trials and evaluated trial quality. RESULTS OF DATA SYNTHESIS: Two Phase III comparative trials evaluating gallium nitrate in the treatment of hypercalcemia of malignancy have been completed. Gallium nitrate was shown to be superior to both calcitonin and etidronate disodium, based on the comparative percentage of patients achieving normocalcemia and the subsequent duration of normocalcemia. Both trials employed similar methodology. Positive therapeutic effects of gallium nitrate have also been demonstrated in small, noncomparative trials for hypercalcemia associated with parathyroid carcinoma, Paget's disease of bone, and osteolytic bone metastases. CONCLUSIONS: Gallium nitrate is effective in the treatment of hypercalcemia associated with malignancy and is appropriate for formulary addition. In certain clinical situations, it may be clearly advantageous over such agents as calcitonin, plicamycin, and etidronate. Further investigation is needed to define the limitations of nephrotoxicity and the therapeutic potential for other indications. Further comparative clinical trials of gallium nitrate versus bisphosphonates and plicamycin could also help define its relative clinical benefit.

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2

Todd, Peter A., and Andrew Fitton. "Gallium Nitrate." Drugs 42, no. 2 (August 1991): 261–73. http://dx.doi.org/10.2165/00003495-199142020-00007.

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3

Chitambar, Christopher R. "Gallium nitrate revisited." Seminars in Oncology 30, no. 2 Suppl 5 (April 2003): 1–4. http://dx.doi.org/10.1016/s0093-7754(03)00169-6.

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4

Warrell, R. P., D. Lovett, F. A. Dilmanian, R. Schneider, and R. T. Heelan. "Low-dose gallium nitrate for prevention of osteolysis in myeloma: results of a pilot randomized study." Journal of Clinical Oncology 11, no. 12 (December 1993): 2443–50. http://dx.doi.org/10.1200/jco.1993.11.12.2443.

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PURPOSE Since osteolysis is a major cause of morbidity in myeloma, we conducted a pilot study to evaluate whether the addition of gallium nitrate to standard antimyeloma treatment could preserve or increase bone mass in patients with osteolytic disease. METHODS Patients stabilized on cytotoxic therapy were randomized to treatment with gallium nitrate for 6 months, or to observation only for the first 6 months followed by gallium nitrate treatment during the subsequent 6 months. Gallium nitrate was administered in monthly cycles by daily subcutaneous injections (30 mg/m2/d) for 2 weeks, followed by 2 weeks with no therapy, supplemented by an intravenous infusion (100 mg/m2/d) for 5 days every other month. RESULTS Paired 6-month comparisons were available for seven observation periods and 13 gallium nitrate treatment periods. Total-body calcium assessed by delayed-gamma neutron activation (DGNA) decreased in four of seven patients during observation, but increased in nine of 13 patients during gallium nitrate treatment; the mean difference in total-body calcium (TBCa) between the two groups at 6 months was 3%. Median regional bone density assessed by dual-photon absorptiometry (DPA) declined by 1.4% in patients under observation (range, +6.7% to -18.3%), but was unchanged during gallium nitrate treatment (median change, 0%; range, -10.5% to +14.4%). The group mean vertebral fracture index assessed by lateral spine x-rays decreased by 27% during observation compared with 2% during gallium nitrate treatment. Mean body height decreased by 0.57 inches in the observation group and .06 inches in the gallium nitrate group. Patient self-assessment of bone pain showed that seven of 12 gallium nitrate-treated patients rated themselves as experiencing major reductions in bone pain, compared with zero of seven patients who were observed. One episode of hypercalcemia occurred in a patient under observation. CONCLUSION Adjuvant treatment with low-dose gallium nitrate attenuates the rate of bone loss in myeloma and may be useful for ameliorating the consequences of skeletal morbidity in patients with cancer-related osteolysis.

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5

Csaky, Karl G., and Rafael C. Caruso. "Gallium Nitrate Optic Neuropathy." American Journal of Ophthalmology 124, no. 4 (October 1997): 567–68. http://dx.doi.org/10.1016/s0002-9394(14)70881-5.

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6

Ho, D. H., J. R. Lin, N. S. Brown, and R. A. Newman. "Bioavailability of gallium nitrate." European Journal of Pharmacology 183, no. 4 (July 1990): 1200. http://dx.doi.org/10.1016/0014-2999(90)94293-7.

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7

Warrell, R. P., W. K. Murphy, P. Schulman, P. J. O'Dwyer, and G. Heller. "A randomized double-blind study of gallium nitrate compared with etidronate for acute control of cancer-related hypercalcemia." Journal of Clinical Oncology 9, no. 8 (August 1991): 1467–75. http://dx.doi.org/10.1200/jco.1991.9.8.1467.

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Hypercalcemia is a major source of morbidity and mortality in patients with cancer. Gallium nitrate and the bisphosphonate, etidronate, are new agents that have recently become available for treatment of this disorder. To directly compare therapeutic effectiveness, we conducted a randomized, double-blind, multicenter study of gallium nitrate compared with etidronate for acute control of cancer-related hypercalcemia. Gallium nitrate was administered by continuous intravenous (IV) infusion at a dose of 200 mg/m2/d. Etidronate was administered as a 4-hour IV infusion at a dose of 7.5 mg/kg. Both drugs were given daily for 5 consecutive days. Eligible patients had persistent moderate-to-severe hypercalcemia (total serum calcium [corrected for serum albumin] greater than or equal to 12.0 mg/dL) after 2 days of hospitalization and IV hydration. Seventy-one patients were randomized and treated. Twenty-eight of 34 patients (82%) who received gallium nitrate achieved normocalcemia compared with 16 of 37 patients (43%) who received etidronate (P less than .001). Patients who received etidronate required significantly greater amounts of IV fluids (P = .04) and more hypocalcemic drug treatment (P less than .05) during the poststudy period than patients who received gallium nitrate. Kaplan-Meier analysis showed a significantly longer median duration of normocalcemia for patients treated with gallium nitrate (8 days v 0 days, P = .0005). A significantly higher proportion of patients treated with gallium nitrate developed asymptomatic hypophosphatemia compared with patients treated with etidronate (97% v 43%, P less than .001). We conclude that gallium nitrate is highly effective and superior to etidronate for acute control of moderate-to-severe cancer-related hypercalcemia.

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8

Venkatachalam, Taracad K., Paul V. Bernhardt, Damion H. R. Stimson, Gregory K. Pierens, Rajiv Bhalla, and David C. Reutens. "A Novel Strategy to Introduce 18F, a Positron Emitting Radionuclide, into a Gallium Nitrate Complex: Synthesis, NMR, X-Ray Crystal Structure, and Preliminary Studies on Radiolabelling with 18F." Australian Journal of Chemistry 71, no. 3 (2018): 81. http://dx.doi.org/10.1071/ch17334.

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A hexan-3,4-dione bis(4N-phenylthiosemicarbazone) gallium nitrate complex was synthesised and the structure was confirmed by NMR studies. The complex was prepared using an appropriately substituted dithiosemicarbazone and sodium methoxide in anhydrous methanol. The structure was further confirmed using single crystal X-ray crystallography. The crystal structure of gallium nitrate complex of diphenylthiosemicarbazone comprise a planar configuration of the tetradentate coordinated thiosemicarbazone with the Ga3+ ion, with the nitrate ligand occupying the apical coordination site. The X-ray structure of the gallium fluoride complex of pentan-2,3-dione bis(4N-phenylthiosemicarbazone) has been determined and confirms exchange of the nitrate can be achieved with fluoride. We show facile exchange of 18F, a positron emitter, to form the 18F-gallium complex under mild conditions, thus providing confirmation that such a transformation can be used to introduce 18F directly into nitrate-coordinated complexes of gallium-thiosemicarbozone complexes, a new labelling strategy for the preparation of imaging agents.

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9

Li, Lei, Hao Chang, Nie Yong, Meixi Li, Yi Hou, and Wei Rao. "Superior antibacterial activity of gallium based liquid metals due to Ga3+ induced intracellular ROS generation." Journal of Materials Chemistry B 9, no. 1 (2021): 85–93. http://dx.doi.org/10.1039/d0tb00174k.

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10

Goodley, Paul H., and Moshe Rogosnitzky. "The Effect of Gallium Nitrate on Arresting Blood Flow from a Wound." Case Reports in Medicine 2011 (2011): 1–3. http://dx.doi.org/10.1155/2011/819710.

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A novel application of gallium nitrate, hitherto unreported, in reducing bleeding time from an open wound is presented. Experiments performed using simple punctures in the forearm demonstrated a very substantial reduction in bleeding time when a solution of gallium nitrate was applied relative to a control. This outcome was shown to be unaffected by the anticoagulant properties of warfarin. The mechanism for such action of gallium nitrate is unknown and merits further investigation, as do the possibilities for such an application to improve both civilian and defense trauma treatment modalities.

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11

Apseloff, Glen. "Therapeutic Uses of Gallium Nitrate." American Journal of Therapeutics 6, no. 6 (November 1999): 327–40. http://dx.doi.org/10.1097/00045391-199911000-00008.

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12

McCaffrey, J. A., S. Hilton, M. Mazumdar, S. Sadan, M. Heineman, J. Hirsch, W. K. Kelly, H. I. Scher, and D. F. Bajorin. "Phase II randomized trial of gallium nitrate plus fluorouracil versus methotrexate, vinblastine, doxorubicin, and cisplatin in patients with advanced transitional-cell carcinoma." Journal of Clinical Oncology 15, no. 6 (June 1997): 2449–55. http://dx.doi.org/10.1200/jco.1997.15.6.2449.

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PURPOSE A phase II randomized trial of gallium nitrate/fluorouracil (5-FU) versus dose-intense methotrexate, vinblastine, doxorubicin, and cisplatin (M-VAC) was performed in poor-risk patients with advanced urothelial tract tumors. The efficacy and toxicity of these regimens were compared. Assessment of dose-intense M-VAC as salvage treatment in patients who failed to respond to the gallium nitrate/5-FU regimen was also performed. PATIENTS AND METHODS Thirty-four patients who had not received prior systemic chemotherapy were randomized to either arm of the study. All patients had one or more clinical features predicting a low likelihood of durable complete response to standard chemotherapy, ie, weight loss, visceral metastases, and low performance status. Gallium nitrate and 5-FU were each administered by continuous 5-day infusions every 28 days. M-VAC was recycled every 21 days, with prophylactic recombinant human granulocyte colony-stimulating factor (rh-G-CSF). RESULTS Two of 17 patients (12%; 95% confidence interval [CI], 1.4% to 36.4%) had a major response to gallium nitrate/5-FU. Sixteen of 17 patients treated with M-VAC (94%; 95% CI, 71.3% to 99.8%) demonstrated a major response. Five of 12 patients who failed to respond to the gallium nitrate/5-FU combination responded to M-VAC as second-line therapy (42%; 95% CI, 15.2% to 72.3%). Median survival for the gallium nitrate and 5-FU arm was 19 versus 17 months for the M-VAC arm, with a median follow-up duration of 35 months (range, 2 to 51) for all patients. Dose-intense M-VAC was associated with a greater incidence of neutropenia and thrombocytopenia. CONCLUSION Dose-intense M-VAC is superior to gallium nitrate/5-FU in poor-risk patients (P < .0001). Despite the overall high response rate, the median survival for patients with M-VAC remained unsatisfactory. Similar survival distributions were observed for patients who received investigational therapy followed by cisplatin-based therapy and patients treated with initial cisplatin-based therapy.

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13

Mori, Graziela Garrido, Roberto Brandão Garcia, Ivaldo Gomes de Moraes, Clóvis Monteiro Bramante, and Norberti Bernardineli. "Morphometric and microscopic evaluation of the effect of gallium nitrate as a root canal dressing in rat teeth submitted to late replantation." Journal of Applied Oral Science 14, no. 6 (December 2006): 405–9. http://dx.doi.org/10.1590/s1678-77572006000600004.

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The purpose of this study was to test a gallium nitrate solution, a resorption inhibitor, employed as a root canal dressing in teeth submitted to late replantation. Thirty maxillary right central incisors of rats were avulsed and kept dry for thirty minutes. The teeth were instrumented and the root surfaces were treated with 1% hypochlorite solution followed by application of 2% sodium fluoride. Thereafter, the teeth were divided into two groups according to the root canal dressing: Group I, solution of gallium nitrate; and Group II, calcium hydroxide paste. The teeth were then replanted in their respective sockets. The animals were killed at 15, 30 and 60 days after replantation and the samples were processed for morphometric and microscopic analysis. The results demonstrated that the gallium nitrate solution and the calcium hydroxide paste limited the root resorption, yet they did not impair its occurrence. It may be concluded that gallium nitrate solution and calcium hydroxide paste demonstrated similar performance.

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14

de Léséleuc, Louis, Greg Harris, Rhonda KuoLee, and Wangxue Chen. "In VitroandIn VivoBiological Activities of Iron Chelators and Gallium Nitrate against Acinetobacter baumannii." Antimicrobial Agents and Chemotherapy 56, no. 10 (July 23, 2012): 5397–400. http://dx.doi.org/10.1128/aac.00778-12.

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ABSTRACTWe investigated the ability of compounds interfering with iron metabolism to inhibit the growth ofAcinetobacter baumannii. Iron restriction with transferrin or 2,2-bipyridyl significantly inhibitedA. baumanniigrowthin vitro. Gallium nitrate alone was moderately effective at reducingA. baumanniigrowth but became bacteriostatic in the presence of serum or transferrin. More importantly, gallium nitrate treatment reduced lung bacterial burdens in mice. The use of gallium-based therapies shows promise for the control of multidrug-resistantA. baumannii.

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15

Okada, H., J. I. Merryman, T. J. Rosol, and C. C. Capen. "Effects of Humoral Hypercalcemia of Malignancy and Gallium Nitrate on Thyroid C Cells in Nude Mice: Immunohistochemical and Ultrastructural Investigations." Veterinary Pathology 31, no. 3 (May 1994): 349–57. http://dx.doi.org/10.1177/030098589403100308.

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Immunohistochemical and ultrastructural investigations of thyroid C cells were conducted in male nude (athymic) mice bearing a serially transplantable canine adenocarcinoma (CAC-8) model of humoral hypercalcemia of malignancy following subcutaneous administration of gallium nitrate. The following four groups were investigated: 1) vehicle-treated non-tumor-bearing control mice; 2) non-tumor-bearing mice treated with gallium nitrate; 3) vehicle-treated hypercalcemic mice bearing CAC-8; and 4) CAC-8 tumor-bearing mice treated with gallium nitrate. Gallium nitrate-treated tumor-bearing mice had a significant decrease in serum calcium as compared with tumor-bearing controls. C cells of non-tumor-bearing mice stained intensely for calcitonin and calcitonin gene-related peptide and weakly for chromogranin A and neuron-specific enolase. In C cells of both vehicle- and gallium-treated tumor-bearing mice, immunoreactive staining was decreased for calcitonin, calcitonin gene-related peptide, and chromogranin A, whereas there was a moderate increase in staining for neuron-specific enolase. Ultrastructurally, thyroid C cells in hypercalcemic tumor-bearing control and gallium-treated mice were hypertrophic and markedly degranulated as compared with those of non-tumor-bearing controls. Hypertrophic C cells contained few mature secretory granules, a well-developed Golgi apparatus, and lamellar arrays of rough endoplasmic reticulum. There was no evidence of C-cell hyperplasia. Immunohistochemical and ultrastructural findings revealed that C cells in mice with cancer-associated hypercalcemia were primarily in the actively synthesizing phase of the secretory cycle and had diminished immunoreactivity for calcitonin, calcitonin gene-related peptide, and chromogranin A. Gallium nitrate did not alter immunohistochemical or ultrastructural features of chronically stimulated C cells even though serum calcium was reduced.

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16

Venkatachalam, T. K., G. K. Pierens, Paul V. Bernhardt, D. H. R. Stimson, R. Bhalla, L. Lambert, and D. C. Reutens. "Heteronuclear NMR Spectroscopic Investigations of Gallium Complexes of Substituted Thiosemicarbazones Including X-Ray Crystal Structure, a New Halogen Exchange Strategy, and 18F Radiolabelling." Australian Journal of Chemistry 69, no. 9 (2016): 1033. http://dx.doi.org/10.1071/ch16044.

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Five thiosemicarbazone ligands have been synthesized, and their coordination chemistry with gallium was investigated. The reaction of these thiosemicarbazones with gallium chloride in alcohol solutions in the presence of a base yielded the corresponding penta-coordinated Ga-Cl metal complexes. In contrast, the reaction of gallium nitrate with the ligands in the presence of alkoxides resulted in the formation of the corresponding Ga-alkoxides, rather than the anticipated Ga-nitrate complex. The crystal structures of gallium chloride and gallium methoxide complexes of diphenylthiosemicarbazone comprise a planar configuration of the tetradentate-coordinated thiosemicarbazone with Ga3+ ion, with the chloride or methoxide groups occupying the apical coordination site. The corresponding ethoxido complex was also prepared in an identical fashion, and NMR analysis confirmed structural similarity to the methoxido complex. Facile halogen exchange reactions of the gallium chloride complexes were achieved by treatment with silver nitrate, followed by addition of KF or KI to generate the gallium fluoride and iodide complexes, respectively. This method of exchange using halogenated inorganic salts aids the preparation of group 13 fluorides, which are notoriously insoluble in organic solvents, for complexation with organic ligands. All compounds have been fully characterized by NMR, and the X-ray crystal structures of two of the complexes are reported. Additionally, the positron-emitting isotope 18F was introduced in the structure of the diphenyl gallium thiosemicarbazone complex.

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17

Chitambar, CR, and D. Sax. "Regulatory effects of gallium on transferrin-independent iron uptake by human leukemic HL60 cells." Blood 80, no. 2 (July 15, 1992): 505–11. http://dx.doi.org/10.1182/blood.v80.2.505.505.

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Abstract Gallium, a pharmacologically important metal, resembles iron with respect to transferrin (Tf) binding and Tf receptor-mediated cellular uptake. In the present study, we examined the effect of gallium on Tf- independent iron uptake by HL60 cells. In contrast to the inhibitory effect of Tf-gallium on Tf-iron uptake, gallium nitrate, in a time-, temperature-, and concentration-dependent manner, stimulated Tf- independent uptake of iron-nitrilotriacetic acid (Fe-NTA). Preexposure of cells to gallium followed by removal of gallium also resulted in sustained stimulation of iron uptake. The anti-Tf receptor monoclonal antibody 42/6 blocked Tf-iron uptake, but had no effect on gallium- induced stimulation of Tf-independent iron uptake. Gallium increased the number of cell membrane iron-binding sites, without a change in their affinity for iron. Ferric chloride stimulated Tf-independent gallium uptake. Although gallium nitrate inhibited cell growth in Tf- free medium, cellular proliferation was restored by Fe-NTA. Gallium and iron appear to share the same Tf-independent cellular uptake system in HL60 cells. Exposure of cells to gallium results in the activation of cell membrane non-Tf iron carriers that may play a role in overcoming the Tf-independent growth-inhibitory effects of gallium.

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18

Chitambar, CR, and D. Sax. "Regulatory effects of gallium on transferrin-independent iron uptake by human leukemic HL60 cells." Blood 80, no. 2 (July 15, 1992): 505–11. http://dx.doi.org/10.1182/blood.v80.2.505.bloodjournal802505.

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Gallium, a pharmacologically important metal, resembles iron with respect to transferrin (Tf) binding and Tf receptor-mediated cellular uptake. In the present study, we examined the effect of gallium on Tf- independent iron uptake by HL60 cells. In contrast to the inhibitory effect of Tf-gallium on Tf-iron uptake, gallium nitrate, in a time-, temperature-, and concentration-dependent manner, stimulated Tf- independent uptake of iron-nitrilotriacetic acid (Fe-NTA). Preexposure of cells to gallium followed by removal of gallium also resulted in sustained stimulation of iron uptake. The anti-Tf receptor monoclonal antibody 42/6 blocked Tf-iron uptake, but had no effect on gallium- induced stimulation of Tf-independent iron uptake. Gallium increased the number of cell membrane iron-binding sites, without a change in their affinity for iron. Ferric chloride stimulated Tf-independent gallium uptake. Although gallium nitrate inhibited cell growth in Tf- free medium, cellular proliferation was restored by Fe-NTA. Gallium and iron appear to share the same Tf-independent cellular uptake system in HL60 cells. Exposure of cells to gallium results in the activation of cell membrane non-Tf iron carriers that may play a role in overcoming the Tf-independent growth-inhibitory effects of gallium.

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19

Sarkar, Sujoy, and S. Sampath. "Ambient temperature deposition of gallium nitride/gallium oxynitride from a deep eutectic electrolyte, under potential control." Chemical Communications 52, no. 38 (2016): 6407–10. http://dx.doi.org/10.1039/c6cc02487d.

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A ternary, ionically conducting, deep eutectic solvent based on acetamide, urea and gallium nitrate is reported for the electrodeposition of gallium nitride/gallium indium nitride under ambient conditions; blue and white light emitting photoluminescent deposits are obtained under potential control.

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20

Bernstein, Lawrence R., Trevor Tanner, Claire Godfrey, and Bruce Noll. "Chemistry and Pharmacokinetics of Gallium Maltolate, a Compound With High Oral Gallium Bioavailability." Metal-Based Drugs 7, no. 1 (January 1, 2000): 33–47. http://dx.doi.org/10.1155/mbd.2000.33.

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Gallium maltolate, tris(3-hydroxy-2-methyl-4H-pyran-4-onato)gallium (GaM), is an orally active gallium compound for therapeutic use. It is moderately soluble in water (10.7 ± 0.9 mg/mL at 25C∘) with an octanol partition coefficient of 0.41±0.08. The molecule is electrically neutral in aqueous solution at neutral pH; a dilute aqueous solution (2.5 ×10−5 M) showed little dissociation at pH 5.5-8.0. Single crystal X-ray diffraction analysis found the GaM molecule to consist of three maltolate ligands bidentately bound to a central gallium atom in a propeller-like arrangement, with one of the ligands disordered in two possible orientations. The compound is orthorhombic, space group Pbca, unit cell a = 16.675(3), b = 12.034(2), c = 18.435(2) A∘ at 158K. GaM was administered to healthy human volunteers at single doses of 100, 200, 300, and 500 mg (three subjects per dose). GaM was very well tolerated. Oral absorption of Ga into plasma was fairly rapid (absorption half life = 0.8-2.0h), with a central compartment excretion half life of 17-21h. Absorption appeared dose proportional over the dosage range studied. Estimated oral gallium bioavailability was approximately 25-57%, based on comparison with published data on intravenous gallium nitrate. Urinary Ga excretion following oral GaM administration was approximately 2% of the administered dose over 72h, in contrast to 49-94% urinary Ga excretion over 24h following i.v. gallium nitrate administration. We suggest that oral administration of GaM results in nearly all plasma gallium being bound to transferrin, whereas i.v. administration of gallium nitrate results in formation of considerable plasma gallate [Ga(OH)4−], which is rapidly excreted in the urine. These data support the continued investigation of GaM as an orally active therapeutic gallium compound.

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21

Warrell, R. P., N. W. Alcock, and R. S. Bockman. "Gallium nitrate inhibits accelerated bone turnover in patients with bone metastases." Journal of Clinical Oncology 5, no. 2 (February 1987): 292–98. http://dx.doi.org/10.1200/jco.1987.5.2.292.

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Bone metastases are a major source of morbidity in patients with cancer. Previously, we found that gallium nitrate was a highly effective treatment for cancer-related hypercalcemia. Laboratory studies have shown that this drug inhibits bone resorption in vitro and that short-term treatment in vivo increases the calcium content of bone. We evaluated the clinical effects of gallium nitrate on biochemical parameters of increased bone turnover in 22 patients with bone metastases. Treatment with gallium nitrate for five to seven days caused a median reduction in 24-hour urinary calcium excretion of 66% relative to baseline measurements (P less than .01). Hydroxyproline (OHP) excretion was also significantly reduced (P less than .01). The greatest reduction in hydroxyprolinuria occurred in patients with high baseline excretion. Ionized serum calcium and serum phosphorous declined significantly after treatment (P less than .01 for each). Serum immunoreactive parathyroid hormone (PTH) increased significantly (P less than .01), as did serum levels of 1,25 (OH)2-vitamin D3 (P less than .05). Urinary phosphorous excretion and serum levels of 25-OH-vitamin D3 were not significantly changed. No major toxic reactions occurred as a result of this treatment. These results indicate that gallium nitrate significantly reduces biochemical parameters associated with accelerated bone turnover and that this agent may be useful for preventing pathologic conditions associated with bone metastases.

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22

Xu, Zhaorong, Xiaolong Zhao, Xiaodong Chen, Zhaohong Chen, and Zhaofan Xia. "Antimicrobial effect of gallium nitrate against bacteria encountered in burn wound infections." RSC Advances 7, no. 82 (2017): 52266–73. http://dx.doi.org/10.1039/c7ra10265h.

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23

Straus, David J. "Gallium nitrate in the treatment of lymphoma." Seminars in Oncology 30, no. 2 Suppl 5 (April 2003): 25–33. http://dx.doi.org/10.1016/s0093-7754(03)00173-8.

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24

Cournot-Witmer, G., A. Bourdeau, M. Lieberherr, C. L. Thil, J. J. Plachot, G. Enault, R. Bourdon, and S. Balsan. "Bone modeling in gallium nitrate-treated rats." Calcified Tissue International 40, no. 5 (September 1987): 270–75. http://dx.doi.org/10.1007/bf02555260.

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25

Drobyski, WR, R. Ul-Haq, D. Majewski, and CR Chitambar. "Modulation of in vitro and in vivo T-cell responses by transferrin- gallium and gallium nitrate." Blood 88, no. 8 (October 15, 1996): 3056–64. http://dx.doi.org/10.1182/blood.v88.8.3056.bloodjournal8883056.

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Gallium is a group IIIa metal that has efficacy in the therapy of malignant disorders such as lymphoma and urothelial tract tumors. Preclinical studies also indicate a role for gallium in autoimmune disorders, suggesting that gallium is able to modulate T-cell immune reactivity. The purpose of this study was to examine the in vitro and in vivo immunomodulatory action of gallium on T-cell function. Since gallium binds to transferrin in vivo, in vitro studies evaluated the effect of transferrin-gallium (Tf-Ga) on human T cells. Tf-Ga inhibited the mitogen-induced proliferative response of peripheral blood mononuclear cells (PBMC) in a dose-dependent fashion. Alloantigen-induced proliferation was also potently suppressed when evaluated in a mixed lymphocyte culture assay. Tf-Ga affected a significant reduction in the density of IL-2 receptors on activated T cells and a slight reduction in the number of CD3+/CD25+ T cells in PHA-stimulated cultures. Neither secretion of interleukin-2 (IL-2) nor the induction of IL-2-stimulated lymphokine-activated killer activity, however, was inhibited by Tf-Ga. Tf-Ga produced significant upregulation of the transferrin receptor (CD71) in T cells as determined by flow cytometric analysis and northern blot assay, but did not affect the percentage of CD3+/ CD71+ T cells after mitogen stimulation. To assess the in vivo effects of gallium on alloreactive T cells, we evaluated the immunosuppressive effect of gallium in a murine model of graft-versus-host disease (GVHD). Administration of gallium significantly prolonged survival in mice undergoing severe GVHD, suggesting that gallium can ameliorate GVH reactivity. Collectively, these data demonstrate that, at clinically achievable concentrations, Tf-Ga potently inhibits T-cell activation and that this immunosuppressive property of gallium may be of adjunctive therapeutic value in the management of disorders characterized by the presence of autoreactive or alloreactive T-cell populations.

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Faulhaber, Sabine, Lars Loeffler, Jerry Hu, Edwin Kroke, Ralf Riedel, and Fred F. Lange. "Synthesis of nanocrystalline aluminum–gallium nitride (AlxGa1−xN; x = 0.1 to 0.5) with oxide precursors via ammonolysis." Journal of Materials Research 18, no. 10 (October 2003): 2350–58. http://dx.doi.org/10.1557/jmr.2003.0329.

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Oxygen-containing precursor systems for the synthesis of mixed aluminum–gallium nitride (AlxGa1−xN with x = 0.1 to 0.5) through ammonolysis (heat treatment under ammonia) were evaluated. Three different precursor systems were studied: (i) aluminum isopropoxide (aluminum sec-butoxide)/gallium isopropoxide hydrolyzed with excess water and cross-linked with 1,6-hexanediol, (ii) aluminum–gallium hydroxide coprecipitated from aluminum–gallium nitrate solution, and (iii) spray-dried aluminum–gallium nitrate solutions. The specimens were heat-treated between 700 °C and 1100 °C and were characterized mainly by x-ray diffraction, nuclear magnetic resonance (NMR), and transmission electron microscopy (TEM). NMR was used to follow the conversion of oxygen to nitrogen bonds. TEM in combination with energy-dispersive x-ray spectroscopy was used to determine the solid-solution composition for separated particles. It is possible to synthesize a mixed hexagonal (Al,Ga)N with crystallite sizes in the range of ∼10 nm from all three precursor systems, but all products contained larger GaN crystals ranging from 20 nm (alkoxide-derived) to 200 nm (hydroxide-derived) and a fraction of untransformed Al–O bonds; e.g., (amorphous or γ-phase) Al2O3.

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Smith, S. E., A. Toor, J. Klein, T. Rodriguez, and P. J. Stiff. "The combination of gallium nitrate, rituximab and dexamethasone is effective and safe as a salvage regimen for diffuse large B-cell lymphoma." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 17510. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.17510.

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17510 Background: More than 56,000 new cases of non-Hodgkin’s lymphoma (NHL) will be diagnosed this year in the United States. As our aging patient population develops worsening performance status and co-morbidities, it seems appropriate to develop effective lymphoma treatments, which have fewer toxicities and lower costs for administration. One approach is to combine non-myelosuppressive therapies. One non-myelosuppressive agent, which has efficacy in lymphoma, is gallium nitrate. Investigation of gallium nitrate for cancer treatment dates back to the 1970’s and it has been shown to inhibit ribonucleotide reductase and bind transferrin and potentially complex with transferrin and/or transferrin receptor, which is highly expressed in intermediate and aggressive histology lymphomas. It appears that the binding of the transferrin receptor on the lymphocyte as well as its inhibition of ribonucleotide reductase, eventually impairs iron metabolism, which is a necessary component of the intracellular cytochrome systems/mitochondrial function and ultimately oxidative phosphorylation. Methods: The current study is a phase II clinical trial investigating the combination of gallium nitrate, rituximab and dexamethasone (GaRD) for relapsed or refractory DLBCL, MCL or transformed follicular lymphomas. The gallium nitrate is given at 200mg/m2 CIV days 1–7, rituximab 375mg/m2 IVPB day 1 and dexamethasone 40 mg po days 1–4. Eligible patients must have proven relapsed or refractory disease and have a SWOG PS ≤3. Patients may have failed prior ASCT or allogeneic SCT. The accrual goal was 37 patients however the study was stopped after 22 patients were accrued as the primary endpoint was reached after the initial interim analysis. Results: ORR 12/22 (55%); CR/CRu 6/22(27%); PR 6/22(27%); SD 3/22 (14%); and PD 7/22 (32%). Most of these patients were refractory to prior salvage regimens 15/22 (68%), including ESHAP, DHAP or high-dose cyclophosphamide. No patients developed grade 3 or 4 toxicities, with the exception of grade 4 lymphopenia. Conclusions: Gallium nitrate, rituximab and dexamethasone (GaRD) appears to be an effective and non-toxic salvage regimen for patients with relapsed DLBCL [Table: see text]

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Mori, Graziela Garrido, Ivaldo Gomes de Moraes, Roberto Brandão Garcia, Lilian Cristina Baraldi Borro, and Bruno Rombaldi Purificação. "Microscopic investigation of the use of gallium nitrate for root surface treatment in rat teeth submitted to delayed replantation." Brazilian Dental Journal 18, no. 3 (2007): 198–201. http://dx.doi.org/10.1590/s0103-64402007000300004.

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The aim of this study was to investigate the effect of gallium nitrate solution, an anti-resorption substance, when applied for root surface treatment in rat teeth submitted to delayed replantation, in order to inhibit the root resorption process and enhance repair. For such purpose, 20 maxillary right central incisors of rats were randomly assigned to 2 groups (n=10). In group I, root surface was treated with 10-4M gallium nitrate solution for 20 min, while in group II root surface was treated with 2% sodium fluoride for 20 min. All root canals were filled with a calcium hydroxide-based paste. At 15 and 60 days after replantation, the animals were killed and the specimens were processed in laboratory for light transmission microscopy. In both groups, there was mild occurrence of ankylosis and root resorption. The connective tissue formed at the periodontal ligament area was arranged parallel to the root in most specimens in both groups and presented signs of inflammation. In group I, there was periodontal pocket formation in all specimens at 60 days, revealing lack of repair. These findings contraindicate the use of gallium nitrate for root surface treatment of teeth submitted to late replantation.

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Chitambar, CR, and Z. Zivkovic. "Inhibition of hemoglobin production by transferrin-gallium." Blood 69, no. 1 (January 1, 1987): 144–49. http://dx.doi.org/10.1182/blood.v69.1.144.144.

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Abstract Recent clinical trials evaluating gallium nitrate as a chemotherapeutic agent have reported the development of microcytic hypochromic anemia in patients treated with this agent. Because gallium is known to bind avidly to transferrin, we examined the effect of transferrin-gallium (Tf-Ga) on hemoglobin production by Friend erythroleukemia cells in vitro. Cellular hemoglobin production, as assessed by benzidine staining, cellular hemoglobin content, and 59Fe incorporation into heme, was significantly decreased following exposure of cells to Tf-Ga. Tf-Ga led to an early decrease in cellular 59Fe incorporation even before changes in hemoglobin production were detected. A marked increase in cellular transferrin receptor expression occurred following exposure of cells to Tf-Ga. Tf-Ga inhibition of hemoglobin production could be reversed and hemoglobin production could be restored to normal by addition to the media of either transferrin-iron (Tf-Fe) or iron- pyridoxal isonicotinoyl hydrazone, a compound capable of supplying iron directly to reticulocytes for heme synthesis without transferrin as a mediator. These studies provide an explanation for the development of anemia in patients treated with gallium nitrate and suggest that gallium's mechanism of chemotherapeutic action includes inhibition of cellular iron incorporation.

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Chitambar, CR, and Z. Zivkovic. "Inhibition of hemoglobin production by transferrin-gallium." Blood 69, no. 1 (January 1, 1987): 144–49. http://dx.doi.org/10.1182/blood.v69.1.144.bloodjournal691144.

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Recent clinical trials evaluating gallium nitrate as a chemotherapeutic agent have reported the development of microcytic hypochromic anemia in patients treated with this agent. Because gallium is known to bind avidly to transferrin, we examined the effect of transferrin-gallium (Tf-Ga) on hemoglobin production by Friend erythroleukemia cells in vitro. Cellular hemoglobin production, as assessed by benzidine staining, cellular hemoglobin content, and 59Fe incorporation into heme, was significantly decreased following exposure of cells to Tf-Ga. Tf-Ga led to an early decrease in cellular 59Fe incorporation even before changes in hemoglobin production were detected. A marked increase in cellular transferrin receptor expression occurred following exposure of cells to Tf-Ga. Tf-Ga inhibition of hemoglobin production could be reversed and hemoglobin production could be restored to normal by addition to the media of either transferrin-iron (Tf-Fe) or iron- pyridoxal isonicotinoyl hydrazone, a compound capable of supplying iron directly to reticulocytes for heme synthesis without transferrin as a mediator. These studies provide an explanation for the development of anemia in patients treated with gallium nitrate and suggest that gallium's mechanism of chemotherapeutic action includes inhibition of cellular iron incorporation.

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31

Carnes, Matthew E., Christopher C. Knutson, Athavan Nadarajah, Milton N. Jackson, Anna F. Oliveri, Kevin M. Norelli, Brandon M. Crockett та ін. "Electrochemical synthesis of flat-[Ga13−xInx(μ3-OH)6(μ-OH)18(H2O)24(NO3)15] clusters as aqueous precursors for solution-processed semiconductors". J. Mater. Chem. C 2, № 40 (2014): 8492–96. http://dx.doi.org/10.1039/c4tc01354a.

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32

&NA;. "Osteolysis of multiple myeloma responds to gallium nitrate." Inpharma Weekly &NA;, no. 920 (January 1994): 18. http://dx.doi.org/10.2165/00128413-199409200-00044.

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33

Whitacre, Caroline, Glen Apseloff, Karen Cox, Velimir Matkovic, Scott Jewell, and Nicholas Gerber. "Suppression of experimental autoimmune encephalomyelitis by gallium nitrate." Journal of Neuroimmunology 39, no. 1-2 (July 1992): 175–81. http://dx.doi.org/10.1016/0165-5728(92)90186-o.

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34

Bockman, Richard. "The effects of gallium nitrate on bone resorption." Seminars in Oncology 30, no. 2 Suppl 5 (April 2003): 5–12. http://dx.doi.org/10.1016/s0093-7754(03)00170-2.

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35

Einhorn, Lawrence. "Gallium nitrate in the treatment of bladder cancer." Seminars in Oncology 30, no. 2 Suppl 5 (April 2003): 34–41. http://dx.doi.org/10.1016/s0093-7754(03)00174-x.

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36

Angulo, SJ, DH Pashley, RJ Loushine, AM Ghazi, and JD Eick. "OR 64 Gallium nitrate diffusion across root dentin." Journal of Endodontics 23, no. 4 (April 1997): 265. http://dx.doi.org/10.1016/s0099-2399(97)80121-5.

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37

LOBANOFF, MARK C., ALEXANDER T. KOZHICH, DANIEL I. MULLET, NICHOLAS GERBER, IGAL GERY, CHI-CHAO CHAN, and SCOTT M. WHITCUP. "Effect of Gallium Nitrate on Experimental Autoimmune Uveitis." Experimental Eye Research 65, no. 6 (December 1997): 797–801. http://dx.doi.org/10.1006/exer.1997.0395.

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38

Rao, S. A., D. W. Palmer, R. S. Hellman, and L. A. Trembath. "Gallium-72 nitrate; a potential radiothbrapbotic skeletal agent." Journal of Labelled Compounds and Radiopharmaceuticals 26, no. 1-12 (January 1989): 369–71. http://dx.doi.org/10.1002/jlcr.25802601159.

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39

Gómez, Mercedes, Domingo J. Sánchez, José L. Domingo, and Jacinto Corbella. "Developmental toxicity evaluation of gallium nitrate in mice." Archives of Toxicology 66, no. 3 (February 1992): 188–92. http://dx.doi.org/10.1007/bf01974013.

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40

Apseloff, G., Kevin V. Hackshaw, Caroline Whitacre, Steven E. Weisbrode, and Nicholas Gerber. "Gallium nitrate suppresses lupus in MRL/lpr mice." Naunyn-Schmiedeberg's Archives of Pharmacology 356, no. 4 (September 16, 1997): 517–25. http://dx.doi.org/10.1007/pl00005085.

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41

Warrell, Raymond P. "Gallium nitrate for the treatment of bone metastases." Cancer 80, S8 (October 15, 1997): 1680–85. http://dx.doi.org/10.1002/(sici)1097-0142(19971015)80:8+<1680::aid-cncr19>3.0.co;2-w.

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42

Kerridge, D. H., and W. M. Shakir. "Molten lithium nitrate-potassium nitrate eutectic: the reactions of aluminium, gallium and thallium." Thermochimica Acta 182, no. 1 (June 1991): 107–22. http://dx.doi.org/10.1016/0040-6031(91)87012-l.

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Antunes, Luísa C. S., Francesco Imperi, Fabrizia Minandri, and Paolo Visca. "In VitroandIn VivoAntimicrobial Activities of Gallium Nitrate against Multidrug-Resistant Acinetobacter baumannii." Antimicrobial Agents and Chemotherapy 56, no. 11 (September 10, 2012): 5961–70. http://dx.doi.org/10.1128/aac.01519-12.

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ABSTRACTMultidrug-resistantAcinetobacter baumanniiposes a tremendous challenge to traditional antibiotic therapy. Due to the crucial role of iron in bacterial physiology and pathogenicity, we investigated iron metabolism as a possible target for anti-A. baumanniichemotherapy using gallium as an iron mimetic. Due to chemical similarity, gallium competes with iron for binding to several redox enzymes, thereby interfering with a number of essential biological reactions. We found that Ga(NO3)3, the active component of an FDA-approved drug (Ganite), inhibits the growth of a collection of 58A. baumanniistrains in both chemically defined medium and human serum, at concentrations ranging from 2 to 80 μM and from 4 to 64 μM, respectively. Ga(NO3)3delayed the entry ofA. baumanniiinto the exponential phase and drastically reduced bacterial growth rates. Ga(NO3)3activity was strongly dependent on iron availability in the culture medium, though the mechanism of growth inhibition was independent of dysregulation of gene expression controlled by the ferric uptake regulator Fur. Ga(NO3)3also protectedGalleria mellonellalarvae from lethalA. baumanniiinfection, with survival rates of ≥75%. At therapeutic concentrations for humans (28 μM plasma levels), Ga(NO3)3inhibited the growth in human serum of 76% of the multidrug-resistantA. baumanniiisolates tested by ≥90%, raising expectations on the therapeutic potential of gallium for the treatment ofA. baumanniibloodstream infections. Ga(NO3)3also showed strong synergism with colistin, suggesting that a colistin-gallium combination holds promise as a last-resort therapy for infections caused by pan-resistantA. baumannii.

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44

Monk, Caroline S., Raymond W. Sweeney, Lawrence R. Bernstein, and Marie-Eve Fecteau. "Serum and tissue concentrations of gallium after oral administration of gallium nitrate and gallium maltolate to neonatal calves." American Journal of Veterinary Research 77, no. 2 (February 2016): 151–55. http://dx.doi.org/10.2460/ajvr.77.2.151.

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Kim, Tae-Hee, Sooseok Choi, and Dong-Wha Park. "Thermal Plasma Synthesis of Crystalline Gallium Nitride Nanopowder from Gallium Nitrate Hydrate and Melamine." Nanomaterials 6, no. 3 (February 24, 2016): 38. http://dx.doi.org/10.3390/nano6030038.

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Graves, Joseph L., Akamu J. Ewunkem, Jason Ward, Constance Staley, Misty D. Thomas, Kristen L. Rhinehardt, Jian Han, and Scott H. Harrison. "Experimental evolution of gallium resistance in Escherichia coli." Evolution, Medicine, and Public Health 2019, no. 1 (January 1, 2019): 169–80. http://dx.doi.org/10.1093/emph/eoz025.

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Abstract Background and Objectives Metallic antimicrobial materials are of growing interest due to their potential to control pathogenic and multidrug-resistant bacteria. Yet we do not know if utilizing these materials can lead to genetic adaptations that produce even more dangerous bacterial varieties. Methodology Here we utilize experimental evolution to produce strains of Escherichia coli K-12 MG1655 resistant to, the iron analog, gallium nitrate (Ga(NO3)3). Whole genome sequencing was utilized to determine genomic changes associated with gallium resistance. Computational modeling was utilized to propose potential molecular mechanisms of resistance. Results By day 10 of evolution, increased gallium resistance was evident in populations cultured in medium containing a sublethal concentration of gallium. Furthermore, these populations showed increased resistance to ionic silver and iron (III), but not iron (II) and no increase in traditional antibiotic resistance compared with controls and the ancestral strain. In contrast, the control populations showed increased resistance to rifampicin relative to the gallium-resistant and ancestral population. Genomic analysis identified hard selective sweeps of mutations in several genes in the gallium (III)-resistant lines including: fecA (iron citrate outer membrane transporter), insl1 (IS30 tranposase) one intergenic mutations arsC →/→ yhiS; (arsenate reductase/pseudogene) and in one pseudogene yedN ←; (iapH/yopM family). Two additional significant intergenic polymorphisms were found at frequencies > 0.500 in fepD ←/→ entS (iron-enterobactin transporter subunit/enterobactin exporter, iron-regulated) and yfgF ←/→ yfgG (cyclic-di-GMP phosphodiesterase, anaerobic/uncharacterized protein). The control populations displayed mutations in the rpoB gene, a gene associated with rifampicin resistance. Conclusions This study corroborates recent results observed in experiments utilizing pathogenic Pseudomonas strains that also showed that Gram-negative bacteria can rapidly evolve resistance to an atom that mimics an essential micronutrient and shows the pleiotropic consequences associated with this adaptation. Lay summary We utilize experimental evolution to produce strains of Escherichia coli K-12 MG1655 resistant to, the iron analog, gallium nitrate (Ga(NO3)3). Whole genome sequencing was utilized to determine genomic changes associated with gallium resistance. Computational modeling was utilized to propose potential molecular mechanisms of resistance.

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Trangwachirachai, Korawich, Chin-Han Chen, Ai-Lin Huang, Jyh-Fu Lee, Chi-Liang Chen, and Yu-Chuan Lin. "Conversion of methane to acetonitrile over GaN catalysts derived from gallium nitrate hydrate co-pyrolyzed with melamine, melem, or g-C₃N₄: the influence of nitrogen precursors." Catalysis Science & Technology 12, no. 1 (2022): 320–31. http://dx.doi.org/10.1039/d1cy01362a.

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The GaN catalyst derived from co-pyrolyzing gallium nitrate hydrate and g-C3N4 is effective in the conversion of methane to acetonitrile because of its well dispersed GaN crystals and amorphous CN species.

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48

Julian, Thomas, Shingai Majuru, Moses Oyewumi, Steven Novick, Miriam Mangelus, Bob Brown, Bharat Mehta, Raymond P. Warrell, and Lewis H. Bender. "Phase 1 Assessment of an Orally Bioavailable Formulation of Gallium Nitrate (G4544)." Blood 110, no. 11 (November 16, 2007): 4455. http://dx.doi.org/10.1182/blood.v110.11.4455.4455.

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Abstract Background: High intravenous doses of gallium nitrate (GN) (200–300 mg/m2/day for 5–7 days) are extremely effective for treatment of patients (pts) with cancer-related hypercalcemia, and preliminary studies have shown consistent anticancer activity in pts with relapsed non-Hodgkin’s lymphoma (NHL). In preclinical studies, low concentrations of GN act as a potent inhibitor of osteoclast-mediated bone resorption, and the agent may also have anabolic effects on bone formation. Clinical studies have shown that low doses of GN (0.25–0.5 mg/kg/day x 14 days) administered by subcutaneous (SC) injection significantly reduced metabolic markers of disordered bone turnover in advanced Paget’s disease. Moreover, a multi-year longitudinal study in pts with advanced multiple myeloma showed that similarly low doses of GN administered by intermittent SC injection significantly reduced bone loss in pts receiving M-2 chemotherapy, and this therapy may have been associated with increased survival (Niesvizky R, Semin Oncol30 (Suppl. 5): 20–4, 2003). GN has low oral bioavailability, and in order to improve dosing convenience over extended periods, we have investigated the oral absorption of numerous gallium-containing compounds. We have successfully developed a novel formulation of GN (G4544) that has acceptable oral bioavailability, and this formulation has now advanced into initial clinical studies. Methods: GN was formulated with a proprietary functional excipient (Emisphere Technologies, Inc.), and compressed into tablets containing 30 mg of elemental gallium by weight (G4544). Oral availability of the formulation was tested in comparison with a control formulation without the functional excipient in dogs. G4544 was then examined in a dose-ranging study to assess safety and pharmacokinetics (PK) following administration of single oral doses to healthy male volunteers. Individual patient cohorts (6 subjects per level) received doses starting at 30 mg gallium and increasing to 60, 90, 120, and 150 mg. Plasma samples were assayed periodically to evaluate PK. Results: Non-clinical studies showed that tablets containing the functional excipient significantly increased gallium absorption compared to controls lacking excipient. The increase in plasma gallium exposure was up to 2.2-fold in AUC and 2.8-fold in Cmax. After a single dose of G4544, the observed mean Cmax and mean AUC0-inf for G4544 was 1.5 ug/mL and 33.0 hr*mg/mL, respectively, compared to 0.5 ug/mL and 14.8 hr*mg/mL for the control formulation. PK assays of clinical samples are pending and will be presented. Conclusions: Low doses of GN have highly potent anti-resorptive effects on bone, and potentially direct activity against myeloma and NHL cells. G4544 markedly increases the oral absorption of GN and may extended oral dosing for treatment of diseases associated with accelerated bone resorption. Follow-up clinical trials are planned to establish the bioequivalence of G4544 to the currently available parenteral formulation for acute treatment of cancer-related hypercalcemia.

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&NA;. "Favourable impact of gallium nitrate in Paget??s disease." Inpharma Weekly &NA;, no. 977 (March 1995): 6. http://dx.doi.org/10.2165/00128413-199509770-00010.

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50

WARRELL, RAYMOND P. "Gallium Nitrate for Acute Treatment of Cancer-Related Hypercalcemia." Annals of Internal Medicine 108, no. 5 (May 1, 1988): 669. http://dx.doi.org/10.7326/0003-4819-108-5-669.

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