ライフサイエンスコーパス: denosumab

1 zoledronic acid and the monoclonal antibody denosumab.

2 consistent with the known safety profile of denosumab.

3 l patients who received at least one dose of denosumab.

4 e patients who received at least one dose of denosumab.

5 by disruption of RANK-RANKL interaction with denosumab.

6 Hypocalcemia occurred more frequently with denosumab.

7 on in bone turnover markers was greater with denosumab.

8 ; hypocalcemia occurred more frequently with denosumab.

9 d patients who received at least one dose of denosumab.

10 and no adverse reactions to the injection of denosumab.

11 phonates or newer targeted therapies such as denosumab.

12 ident three days after the administration of denosumab.

13 0 years of treatment with bisphosphonates or denosumab.

14 toxic effects did not differ with or without denosumab.

15 RONJ significantly earlier when treated with denosumab.

16 CE in reducing the risks of SRE than monthly denosumab.

17 n and more reasonable alternative to monthly denosumab.

18 e compact bone erosion that was prevented by Denosumab.

19 xtension, in which all participants received denosumab.

20 RCA1-mutation carriers who were treated with denosumab.

21 al drugs, especially the bone antiresorptive denosumab.

22 osis of the jaw occurred infrequently (2.0%, denosumab; 1.4%, zoledronic acid; P = .39).

23 omly assigned to receive either subcutaneous denosumab 120 mg and intravenous placebo (n = 1,026) or

24 andomly assigned 1:1 to monthly subcutaneous denosumab 120 mg or placebo.

25 oice response system to receive subcutaneous denosumab 120 mg or subcutaneous placebo every 4 weeks.

26 ast cancer with evidence of bone metastases; denosumab 120 mg subcutaneously every 4 weeks, intraveno

27 sation list (block size 4) to receive either denosumab (120 mg) or matching placebo subcutaneously ev

28 ts were randomized to receive or not receive denosumab, 120 mg subcutaneously every 4 weeks for 6 cyc

29 Options include denosumab, 120 mg subcutaneously, every 4 weeks; pamidro

30 The analyses included 252 patients (132, denosumab; 120, placebo) with a baseline and at least on

31 dustry were associated with increased use of denosumab (17.5% (95% confidence interval 15.3% to 19.7%

32 acebo (n = 75), denosumab 60 mg (n = 71), or denosumab 180 mg (n = 72) injections every 6 months for

33 % [2.9]; teriparatide, 0.7% [2.7], p<0.0001; denosumab 2.5% [2.6], p=0.0011).

34 the teriparatide (0.8% [4.1], p=0.0007) and denosumab (2.1% [3.8], p=0.0238) groups, as did total-hi

35 rall survival did not differ between groups (denosumab, 43.9 [95% CI 40.1-not estimable] months vs pl

36 n the teriparatide (6.2% [4.6], p=0.0139) or denosumab (5.5% [3.3], p=0.0005) groups.

37 to receive placebo (n = 125) or subcutaneous denosumab 60 mg (n = 127) every 6 months.

38 ents received subcutaneous placebo (n = 75), denosumab 60 mg (n = 71), or denosumab 180 mg (n = 72) i

39 whom 3420 were randomly assigned to receive denosumab 60 mg (n=1711) or placebo (n=1709) subcutaneou

40 At 3 months, both groups were started on denosumab 60 mg every 6 months via subcutaneous injectio

41 ly assigned in a 1:1 ratio to receive either denosumab 60 mg or placebo administered subcutaneously e

42 Adjuvant denosumab 60 mg twice per year reduces the risk of clini

43 e undergoing adjuvant treatment with AIs and denosumab (60 mg every 6 months) were enrolled at the Br

44 ive 24 months of teriparatide (20 mg daily), denosumab (60 mg every 6 months), or both drugs.

45 elocity >2.5 m/s) were randomized 2:1:2:1 to denosumab (60 mg every 6 months), placebo injection, ale

46 Denosumab, 60 mg, or oral bisphosphonates.

47 dustry were associated with increased use of denosumab (7.4% (2.5% to 12.2%)) and nab-paclitaxel (1.7

48 e randomly assigned to treatment groups (716 denosumab, 716 placebo).

49 h zoledronic acid (a bisphosphonate) or with denosumab (a monoclonal antibody to RANK ligand) reduces

50 We assessed denosumab, a fully human anti-RANKL monoclonal antibody,

51 This study compared denosumab, a fully human monoclonal anti-receptor activa

52 This randomized study compared denosumab, a fully human monoclonal antibody against rec

53 We investigated the effects of denosumab, a fully human monoclonal antibody against rec

54 We investigated the ability of denosumab, a fully human monoclonal antibody against rec

55 Denosumab, a fully human monoclonal antibody to receptor

56 Denosumab, a fully human mononoclonal antibody to recept

57 Denosumab, a humanized monoclonal antibody against recep

58 onally, data demonstrated the superiority of denosumab, a RANK-ligand antagonist, compared to zoledro

59 In this randomized clinical trial, denosumab added to anthracycline/taxane-based NACT did n

60 to both received an additional 24 months of denosumab alone (combination to denosumab group).

61 Denosumab also consistently increased time to bone metas

62 Denosumab also reduced the risk of nonvertebral fracture

63 Denosumab also reduces risk for radiographic vertebral f

64 Denosumab also significantly delayed time to first bone

65 Denosumab (AMG 162), a fully human monoclonal antibody t

66 Denosumab, an anti-RANK ligand monoclonal antibody, sign

67 ble, including antiresorptive agents such as denosumab and bisphosphonates, as well as complementary

68 of anti-osteoporosis medications, including denosumab and bone-forming therapies.

69 In patients with kidney failure, denosumab and dialysis may be indicated.

70 f adverse events were comparable between the denosumab and placebo groups.

71 Denosumab and radium-223 reduce the risk of skeletal-rel

72 In the Denosumab and Teriparatide Administration (DATA) study,

73 ATA-Switch) is a preplanned extension of the denosumab and teriparatide administration study (DATA),

74 Denosumab and toremifene (a selective estrogen receptor

75 ypocalcaemia occurred in 12 (2%) patients on denosumab and two (<1%) on placebo.

76 high-strength evidence that bisphosphonates, denosumab, and teriparatide reduce fractures compared wi

77 d haematology), and participant incidence of denosumab antibody formation.

78 resorptive agents such as bisphosphonates or denosumab are recommended for patients at high fracture

79 nts (bisphosphonates or, if contraindicated, denosumab) are recommended to reduce vertebral fractures

80 can be used, ranging from bisphosphonates to denosumab, as well as teriparatide.

81 dy, we randomly assigned patients to receive denosumab at a dose of 60 mg subcutaneously every 6 mont

82 logic agent is indicated, bisphosphonates or denosumab at osteoporosis-indicated dosages are the pref

83 porotic women switching from teriparatide to denosumab, bone mineral density continued to increase, w

84 Denosumab can also be considered for the treatment of mu

85 Denosumab caused sustained suppression of markers of bon

86 andomly assigned to one of six cohorts (five denosumab cohorts [blinded to dose and frequency]; one o

87 We aimed to assess whether denosumab combined with standard-of-care adjuvant or neo

88 th prediabetes appeared to benefit more from denosumab compared with an oral bisphosphonate (hazard r

89 e generally similar in patients treated with denosumab compared with those receiving placebo or alend

90 sphosphonates, teriparatide, raloxifene, and denosumab) compared with placebo, usual care, or active

91 Denosumab consistently improves BMFS in men with shorter

92 In analyses by shorter baseline PSADT, denosumab consistently increased BMFS by a median of 6.0

93 Hence denosumab could represent a novel therapeutic approach f

94 gs interfering with RANKL signaling, such as Denosumab, could increase patient survival if used as ad

95 by advances in fundamental bone biology (eg, denosumab) coupled with clues from patients with rare bo

96 adverse events for all individuals receiving denosumab decreased from 165.3 to 95.9 per 100 participa

97 In infertile men, one dose of Denosumab decreases RANKL seminal fluid concentration an

98 Additionally, patients treated with denosumab developed MRONJ significantly earlier.

99 33 (5%) patients on denosumab developed osteonecrosis of the jaw versus none

100 th early-stage breast cancer, in this study, denosumab did not improve disease-related outcomes for w

101 Denosumab discontinuation is challenging due to the rebo

102 in inhibitors, immune checkpoint inhibitors, denosumab discontinuation, SARS-CoV-2, ketogenic diets,

103 ) had hypercalcaemia occurring 30 days after denosumab discontinuation.

104 Here we utilize osteoclast ablation by denosumab (DMAb) and RNA-sequencing of bone biopsies fro

105 inst RANKL-expressing malignant cells and as denosumab does not stimulate NK reactivity, we generated

106 Subjects were randomly assigned to receive denosumab either every three months (at a dose of 6, 14,

107 orts 1 and 2 received 120 mg of subcutaneous denosumab every 4 weeks with loading doses on days 8 and

108 to receive 20 mug teriparatide daily, 60 mg denosumab every 6 months, or both.

109 The data represent up to 10 years of denosumab exposure for women who received 3 years of den

110 CM led to a relative reduction in the use of denosumab for beneficiaries with bone metastases receivi

111 non-recommended or low value interventions: denosumab for castration sensitive prostate cancer, gran

112 w-risk chemotherapy (7.3% v 8.9%; P < .001), denosumab for CSPC (26.4% v 33.1%; P < .001), nab-paclit

113 ose who transferred from a previous study of denosumab for GCTB (cohort 3).

114 ), or were enrolled from a previous study of denosumab for GCTB (cohort 3).

115 Adult patients who received denosumab for osteoporosis therapy in Taiwan between 201

116 clinical data on the efficacy and safety of denosumab for the treatment of postmenopausal osteoporos

117 The fully human monoclonal antibody denosumab (formerly known as AMG 162) binds RANKL with h

118 Administration (DATA) study, we showed that denosumab fully inhibits teriparatide-induced bone resor

119 Denosumab given subcutaneously twice yearly for 36 month

120 density was unchanged in the teriparatide to denosumab group (0.0% [95% CI -1.3 to 1.4]), whereas it

121 se of study drug) did not differ between the denosumab group (1366 events, 80%) and the placebo group

122 ensity increased more in the teriparatide to denosumab group (6.6% [95% CI 5.3-7.9]) than in the deno

123 ensity increased more in the teriparatide to denosumab group (8.3% [95% CI 6.1-10.5]) and the combina

124 the greatest increase in the combination to denosumab group (8.6% [7.1-10.0]; p=0.0446 vs the teripa

125 3% [95% CI 6.1-10.5]) and the combination to denosumab group (9.1% [6.1-12.0]) than in the denosumab

126 The overall lower number of fractures in the denosumab group (92) than in the placebo group (176) was

127 0.118) and significantly lower in the 180-mg denosumab group (mean change 0.06; P = 0.007) than in th

128 n score from baseline was lower in the 60-mg denosumab group (mean change 0.13; P = 0.118) and signif

129 observed as early as 6 months in the 180-mg denosumab group (P = 0.019) as compared with placebo, an

130 ased by 2.8% (1.2-4.4) in the combination to denosumab group (p=0.0075 for the teriparatide to denosu

131 Differences between the combination to denosumab group and the teriparatide to denosumab group

132 he lumbar spine had increased by 5.6% in the denosumab group as compared with a loss of 1.0% in the p

133 n to denosumab group and the teriparatide to denosumab group did not differ significantly (p=0.67).

134 extension, similar to rates observed in the denosumab group during the first three years of the FREE

135 ared with the placebo group, patients in the denosumab group had a significantly delayed time to firs

136 identified more infections (n = 146) in the denosumab group than in the control group (n = 99).

137 eased by 5.5% and 7.6%, respectively, in the denosumab group versus placebo (P < .0001 at both time p

138 ratide group, p=0.30 for the teriparatide to denosumab group vs the combination to denosumab group, a

139 umab group (p=0.0075 for the teriparatide to denosumab group vs the combination to denosumab group; p

140 comparisons, p=0.13 for the teriparatide to denosumab group vs the denosumab to teriparatide group,

141 during the study, of which one death (in the denosumab group) was thought to be related to the study

142 paratide received denosumab (teriparatide to denosumab group), those originally assigned to denosumab

143 to teriparatide group vs the combination to denosumab group).

144 to teriparatide group vs the combination to denosumab group).

145 24 months of denosumab alone (combination to denosumab group).

146 4.9-21.8) in 27 women in the teriparatide to denosumab group, 14.0% (10.9-17.2) in 27 women the denos

147 14.0-18.0) in 23 women in the combination to denosumab group, although this increase did not differ s

148 ide to denosumab group vs the combination to denosumab group, and p=0.41 for the denosumab to teripar

149 [7.1-10.0]; p=0.0446 vs the teriparatide to denosumab group, p<0.0001 vs the denosumab to teriparati

150 , with a cumulative incidence of 0.7% in the denosumab group, versus 1.2% in the placebo group (hazar

151 , with a cumulative incidence of 2.3% in the denosumab group, versus 7.2% in the placebo group (risk

152 , with a cumulative incidence of 6.5% in the denosumab group, versus 8.0% in the placebo group (hazar

153 ide to denosumab group vs the combination to denosumab group; p=0.0099 for the denosumab to teriparat

154 reduction in uNTx/Cr was 71% for the pooled denosumab groups and 79% for the IV BP group.

155 60-mg (P = 0.012) and the 180-mg (P = 0.007) denosumab groups were significantly different from the p

156 Patients who received denosumab had a decreased incidence of new vertebral fra

157 Discontinuing teriparatide and denosumab, however, results in rapidly declining bone mi

158 Both bisphosphonates and denosumab improve BMD in men with nonmetastatic prostate

159 Denosumab improved BMD and reduced the incidence of new

160 In turn a neutralizing Ab against RANKL, denosumab improves bone strength in osteoporosis.

161 8 patients who received at least one dose of denosumab in cohort 2 had no surgery in the first 6 mont

162 b exposure for women who received 3 years of denosumab in FREEDOM and continued in the extension (lon

163 placebo group and the efficacy and safety of denosumab in men with PSADT </= 10, </= 6, and </= 4 mon

164 ficacy and safety of five dosing regimens of denosumab in patients with breast cancer-related bone me

165 and efficacy results from a phase 2 study of denosumab in patients with GCTB.

166 y aimed to assess the safety and activity of denosumab in patients with surgically salvageable or uns

167 the effects of the anti-RANK ligand antibody denosumab in postmenopausal, aromatase inhibitor-treated

168 Comparably, pre-operative single-agent denosumab in premenopausal early-stage breast cancer pat

169 r primary endpoint was the safety profile of denosumab in terms of adverse events and laboratory abno

170 eived 3 years of placebo and transitioned to denosumab in the extension (crossover group).

171 s-dependent patients, the high risk posed by denosumab in this population, and the complex strategies

172 ibition of RANKL signaling by treatment with denosumab in three-dimensional breast organoids derived

173 f monthly ZA, ZA every 3 months, and monthly denosumab in women with breast cancer and skeletal metas

174 Combined teriparatide and denosumab increased BMD more than either agent alone and

175 In postmenopausal women with low bone mass, denosumab increased bone mineral density and decreased b

176 study showed that combined teriparatide and denosumab increased bone mineral density more than eithe

177 Both OPG and denosumab increased limb force proportionally to the inc

178 bined treatment with teriparatide 40 mug and denosumab increases spine and hip BMD more than standard

179 teoprotegerin and the anti-osteoporotic drug denosumab, induces rodent and human beta cell proliferat

180 Denosumab is a fully human monoclonal antibody that bind

181 Denosumab is a fully human monoclonal antibody to the re

182 Denosumab is a fully human monoclonal IgG2 antibody that

183 Denosumab is a novel alternative to bisphosphonates agai

184 Denosumab is a promising therapeutic agent for the manag

185 Denosumab is an investigational fully human monoclonal a

186 opausal women with low bone mineral density, denosumab is associated with a greater increase in bone

187 Denosumab is shown to support bone mineral density in ho

188 In the case of denosumab, it is now apparent that stopping therapy at a

189 itor therapy, twice-yearly administration of denosumab led to significant increases in BMD over 24 mo

190 Data for adjuvant denosumab look promising but are currently insufficient

191 Inhibition of RANK using the approved drug denosumab may be a therapeutic drug candidate for primar

192 Subcutaneous denosumab may be similar to IV BPs in suppressing bone t

193 Given its unique actions, denosumab may be useful in the treatment of osteoporosis

194 Denosumab may delay worsening of pain compared with bisp

195 and beta-cell proliferation, suggesting that denosumab may improve glucose homeostasis; however, whet

196 patients (30.2%) at risk for non-recommended denosumab (median $63), 76 747 of 271 485 patients (28.3

197 in patients who received radium-223 without denosumab (median 13 months, 12-NA).

198 and in patients who received radium-223 plus denosumab (median NA, 15 months-NA) than in patients who

199 ted with RANK expression and was impaired by Denosumab-mediated disruption of the RANK/RANKL loop.

200 These preliminary data suggest that denosumab might be an effective treatment for osteoporos

201 Adjuvant denosumab might improve disease-free survival in hormone

202 Denosumab might prolong progression-free survival in pat

203 4509 women were randomly assigned to receive denosumab (n=2256) or placebo (n=2253) and included in t

204 d received the allocated trial intervention: denosumab (n=49), alendronic acid (n=51), and placebo (i

205 Neither denosumab nor alendronic acid affected progression of ao

206 o serious or fatal adverse events related to denosumab occurred.

207 Effects of teriparatide and denosumab on BMD and fractures are unclear (very low SOE

208 ed clinical trial which tested the effect of denosumab on bone mineral density, we assessed the impac

209 There was no evidence of an effect of denosumab on joint space narrowing or on measures of RA

210 hase II study was to evaluate the effects of denosumab on structural damage in patients with rheumato

211 ents shortly after transplantation to either denosumab on top of standard treatment (calcium and vita

212 Patients received 120 mg subcutaneous denosumab once every 4 weeks during the treatment phase,

213 surgery while medicated with bisphosphonate, denosumab or anti-angiogenic agents.

214 years or older who initiated treatment with denosumab or oral bisphosphonates from 2013 to 2020.

215 assigned (1:1) to receive 60 mg subcutaneous denosumab or placebo every 6 months for 3 years.

216 randomly assigned to receive either 60 mg of denosumab or placebo subcutaneously every 6 months for 3

217 In women, denosumab over 3 years improved appendicular lean mass a

218 In the active treatment comparisons, denosumab, parathyroid hormone receptor agonists, and ro

219 leted (zoledronic acid) or are currently in (denosumab) phase III trials.

220 leted (zoledronic acid) or are currently in (denosumab) phase III trials.

221 Osteoprotegerin and denosumab protected beta cells against this cytotoxicity

222 e incremental costs per mean SRE avoided for denosumab ranged from $162,918 to $347,655.

223 nosumab group), those originally assigned to denosumab received teriparatide (denosumab to teriparati

224 In human immune cells, osteoprotegerin and denosumab reduce proinflammatory cytokines in activated

225 Bisphosphonates (generic) and denosumab reduce the risk of hip, nonvertebral, and vert

226 Osteoprotegerin and denosumab reduced T1D serum-induced beta cell cytotoxici

227 Denosumab reduced the risk of hip fracture, with a cumul

228 As compared with placebo, denosumab reduced the risk of new radiographic vertebral

229 Denosumab reduces bone turnover markers and increases bo

230 mprove glucose homeostasis; however, whether denosumab reduces the risk of incident diabetes remains

231 Denosumab represents a new treatment option for patients

232 Denosumab represents a potential novel treatment option

233 ion and no requirement for renal monitoring, denosumab represents a potential treatment option for pa

234 th concomitant abiraterone, enzalutamide, or denosumab require confirmation in prospective randomised

235 ther Novartis or Amgen, the makers of ZA and denosumab, respectively.

236 cells with the clinically available RANKL Ab Denosumab resulted in enhanced NK cell anti-leukemia rea

237 ed to monitor and treat severe hypocalcemia, denosumab should be administered after careful patient s

238 Denosumab significantly increased bone-metastasis-free s

239 Sensitivity analyses were performed where denosumab SRE probabilities were assumed to be 50%, 75%,

240 isphosphonate, zoledronic acid (ZA), and the denosumab surrogate for rodents, OPG-Fc, in a rat model

241 originally assigned to teriparatide received denosumab (teriparatide to denosumab group), those origi

242 ection (cystitis) occurred more often in the denosumab than in the control group (51 vs 25 episodes i

243 Denosumab therapy was also associated with significant i

244 men treated with alendronate are switched to denosumab, there is an increase in bone mineral density

245 be substantially reduced by the addition of denosumab, this treatment should be considered for clini

246 Both bisphosphonates and denosumab, through different pathways of action, signifi

247 ter displayed similar capacity compared with denosumab to neutralize the effects of RANKL on osteocla

248 Addition of twice-yearly injections of denosumab to ongoing methotrexate treatment inhibited st

249 ost hoc analysis reveals that treatment with denosumab to prevent bone loss in first-year kidney tran

250 lendronate, risedronate, zoledronic acid, or denosumab to reduce the risk for hip and vertebral fract

251 ab group (6.6% [95% CI 5.3-7.9]) than in the denosumab to teriparatide group (2.8% [1.3-4.2], p=0.000

252 enosumab group (9.1% [6.1-12.0]) than in the denosumab to teriparatide group (4.9% [2.2-7.5]; p=0.044

253 One participant in the denosumab to teriparatide group had nephrolithiasis, cla

254 ination to denosumab group; p=0.0099 for the denosumab to teriparatide group vs the combination to de

255 ation to denosumab group, and p=0.41 for the denosumab to teriparatide group vs the combination to de

256 assigned to denosumab received teriparatide (denosumab to teriparatide group), and those originally a

257 paratide to denosumab group, p<0.0001 vs the denosumab to teriparatide group).

258 mab group, 14.0% (10.9-17.2) in 27 women the denosumab to teriparatide group, and 16.0% (14.0-18.0) i

259 s it decreased by -1.8% (-5.0 to 1.3) in the denosumab to teriparatide group, and increased by 2.8% (

260 r the teriparatide to denosumab group vs the denosumab to teriparatide group, p=0.30 for the teripara

261 ontinued to increase, whereas switching from denosumab to teriparatide results in progressive or tran

262 de, p=0.0336 for combination to denosumab vs denosumab to teriparatide).

263 ]; p=0.0447 for teriparatide to denosumab vs denosumab to teriparatide, p=0.0336 for combination to d

264 Overall, 74% of denosumab-treated patients (157 of 211) achieved a more

265 On-study SREs were experienced by 9% of denosumab-treated patients (20 of 211) versus 16% of bis

266 In the unweighted cohorts, 607 of 1523 denosumab-treated patients and 23 of 1281 oral bisphosph

267 Denosumab treatment for 12 months resulted in an increas

268 INTERPRETATION: Denosumab treatment for up to 10 years was associated wi

269 t that the overall risk to benefit ratio for denosumab treatment in patients with GCTB remains favour

270 Results The mean costs of the denosumab treatment strategy are nine-fold higher than g

271 Compared with the comparison group, denosumab treatment was associated with a lower risk of

272 Bone turnover markers decreased with denosumab treatment.

273 In this population based study, denosumab use was associated with a lower risk of incide

274 fractures (odds ratio 1.85, 1.18 to 2.92 for denosumab v parathyroid hormone receptor agonists and 1.

275 receptor agonists and 1.56, 1.02 to 2.39 for denosumab v romosozumab).

276 ed in 122 (5%) of 2241 patients treated with denosumab versus four (<1%) of 2218 patients treated wit

277 investigational product (2241 patients with denosumab vs 2218 patients with placebo), were neutropen

278 to teriparatide, p=0.0336 for combination to denosumab vs denosumab to teriparatide).

279 4.9% [2.2-7.5]; p=0.0447 for teriparatide to denosumab vs denosumab to teriparatide, p=0.0336 for com

280 Denosumab was administered subcutaneously every 4 weeks

281 Denosumab was associated with a markedly higher incidenc

282 Initiation of denosumab was associated with a reduced risk of type 2 d

283 Denosumab was associated with increased bone mineral den

284 Denosumab was associated with tumour responses and reduc

285 While denosumab was found to reduce fractures, long-term survi

286 d hormone receptor agonists and romosozumab, denosumab was less effective in reducing clinical fractu

287 the co-administration of zoledronic acid or denosumab was mandatory.

288 Denosumab was noninferior (trending to superiority) to Z

289 Denosumab was noninferior to ZA in delaying time to firs

290 Although directionally favorable, denosumab was not statistically superior to ZA in delayi

291 Denosumab was superior to zoledronic acid in delaying or

292 Denosumab was superior to zoledronic acid in delaying ti

293 Cabazitaxel, sipuleucel-T and denosumab were approved in 2010 by regulatory agencies i

294 cy and safety of subcutaneously administered denosumab were evaluated over a period of 12 months in 4

295 4301 new users of denosumab were matched on propensity score to 21 038 use

296 ly higher, especially for patients receiving denosumab, when compared with available data in the lite

297 assess the long-term safety and efficacy of denosumab, which is widely used for the treatment of pos

298 consistent with the known safety profile of denosumab, which showed long-term disease control for pa

299 We compared combined teriparatide and denosumab with both agents alone.

300 We aimed to assess whether administration of denosumab with high dose teriparatide would stimulate la

301 tios and 95% confidence intervals, comparing denosumab with oral bisphosphonates using an as treated