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1 non-U.S.-approved formulations (neridronate, clodronate).
2 ) group 5 = diabetes + periodontitis + LDD + clodronate.
3 tive intratracheal instillation of liposomal clodronate.
4 y subconjunctival (SC) delivery of liposomal clodronate.
5 gues and the antimacrophage agent, liposomal clodronate.
6 etion of alveolar macrophages with liposomal clodronate.
7 y treating B6 mice with liposomes containing clodronate.
8 n after macrophage depletion using liposomal clodronate.
9 hibited by the antiosteolytic bisphosphonate clodronate.
10 travenous injection of liposome-encapsulated clodronate.
11 effects were indistinguishable from those of clodronate.
12 antiresorptive and antimacrophage effects of clodronate.
13 ker); and intravenous injection of liposomal clodronate.
14 IL17RA(-/-) mice using liposomes loaded with clodronate.
17 acid (4 mg intravenously every 6 months) or clodronate (1,600 mg/d orally) be considered as adjuvant
18 domly assigned in a 1:1 ratio to either oral clodronate 1600 mg daily for 3 years (n=1662) or placebo
19 igned to take four tablets per day of sodium clodronate (2080 mg) or matching placebo for up to 3 yea
20 ld C57BL/10J mice with liposome-encapsulated clodronate 48 h before 35 min of hepatic ischemia with b
21 ither phosphate-buffered saline (control) or clodronate (a macrophage depleting drug) at 15 weeks pos
22 crophage depletion via liposomal delivery of clodronate, a first-generation bisphosphonate, mitigates
23 re-treatment of the recipient with liposomal clodronate, a macrophage depleting agent, with the goal
26 c cells by injection of liposomes containing clodronate abolished diabetes, although inflammation rem
28 M using intracerebroventricular injection of clodronate abrogates the reactive oxygen species product
29 cant benefits for zoledronic acid (ZOL) over clodronate acid (CLO) were seen in the Medical Research
31 owever, treatment with liposome-encapsulated clodronate, an agent that depletes macrophages in vivo,
32 controlled trials assessed the use of sodium clodronate, an oral, first-generation bisphosphonate.
39 evaluate the effect of mono and combined BP clodronate and LDD therapies in reducing gingival levels
40 aims of this study were to determine whether clodronate and liposome-encapsulated clodronate are meta
41 ause there are no direct comparisons between clodronate and pamidronate or zoledronic acid, the super
42 Most studies evaluated zoledronic acid or clodronate, and data are extremely limited for other bis
43 were depleted from mice by administration of clodronate, and their location and phenotype were examin
44 y the positive result of one trial of sodium clodronate, and we found no evidence of a benefit from t
45 x vivo with immunomagnetic beads) metabolize clodronate, and whether rat peritoneal macrophages metab
46 LDD; 4) group 4 = diabetes + periodontitis + clodronate; and 5) group 5 = diabetes + periodontitis +
47 whether clodronate and liposome-encapsulated clodronate are metabolized to adenosine 5'-(beta,gamma-d
48 ronate, risedronate, and lovastatin, but not clodronate, are blocked by geranylgeraniol, a precursor
49 acerebral injection of liposome-encapsulated clodronate at P5 significantly reduced vessel coverage a
50 he intratracheal administration of liposomal clodronate attenuated particulate matter-induced IL-6 pr
51 B6) mice by i.v. administration of liposomal clodronate before allogeneic bone marrow transplantation
52 in the airways were depleted using liposomal clodronate before infection, this resulted in a signific
53 ection of the macrophage-depleting liposomal clodronate before radiotherapy can increase the antitumo
54 acerebral injection of liposome-encapsulated clodronate before transient middle cerebral artery occlu
57 protocol B-34 aims to ascertain whether oral clodronate can improve outcomes in women with primary br
59 mokine receptor type 2 (CCR2) antagonist and clodronate (CLD) were respectively administered to N12W
60 gimens and IV zoledronic acid (ZOL) and oral clodronate (CLO) in 1960 patients with newly diagnosed m
61 ence of improvement in overall survival with clodronate compared with placebo (HR 1.12, 0.89-1.42; p=
62 e with metastatic disease from use of sodium clodronate compared with placebo was seen in overall sur
64 ippostrongylus brasiliensis and treated with clodronate-containing liposome to deplete macrophages or
65 capsular sinus CD169-positive macrophages by clodronate-containing liposome was associated with a lac
67 rophages using subconjunctival injections of clodronate-containing liposomes before corneal infection
69 normally developed spleens by treatment with clodronate-containing liposomes demonstrated that these
71 macrophages by intranasal administration of clodronate-containing liposomes in caspase-9 inhibitor-t
74 ed mice and compared tumor development using clodronate-containing liposomes to deplete macrophages i
76 Treatment of PVC-211 MuLV-infected rats with clodronate-containing liposomes, which specifically kill
81 splenic phagocytic APCs by i.v. injection of clodronate- (dichloromethylene diphosphonate) containing
83 which is based on intracerebral injection of clodronate disodium salt (CDS) into the PFC of adolescen
85 ival administration of liposome-encapsulated clodronate efficiently diminished resident ocular surfac
86 eolar macrophages were depleted with inhaled clodronate, ELD607 was no longer able to resolve inflamm
87 al macrophages with the macrophagicidal drug clodronate eliminated the latex beads' protective effect
90 hamsters were treated, intratracheally, with clodronate-encapsulated liposomes or control liposomes a
95 s or older on study entry showed benefits of clodronate for recurrence-free interval (0.75, 0.57-0.99
99 tion was noted in 23 of 1612 patients in the clodronate group and 12 of 1623 patients in the placebo
102 not differ between groups (286 events in the clodronate group vs 312 in the placebo group; hazard rat
104 intracebroventricular injection of liposomal clodronate, had little or no effect on the response of l
105 at a first-generation bisphosphonate, sodium clodronate, improves overall survival in men with metast
107 e infiltration by systemic administration of clodronate-incorporated liposomes fails to suppress LSI-
111 (CB(1)R) inverse agonist (SR141716), and by clodronate-induced myeloid-cell depletion, but not by ge
112 Interestingly, macrophage depletion with clodronate inhibited the development of colitis, while t
114 re generated by the combination of liposomal clodronate injection, irradiation, and BM transplantatio
115 lled trials is modest but supports that oral clodronate, intravenous pamidronate, and intravenous zol
116 ted CCR2 chimeric mice by the combination of clodronate, irradiation, and bone marrow (BM) transplant
118 hese results provide proof-of-principle that clodronate is effective at sparing the number of donor B
120 somiasis with macrophage-depleting liposomal clodronate (LC) to define how macrophages mediate bladde
122 owed that delaying macrophage recruitment by clodronate liposome (-1d_CL, macrophage-delayed model) i
123 in the induction of LPC proliferation using clodronate liposome deletion of Kupffer cells and adopti
135 phages, through subconjunctival injection of clodronate liposome, attenuated lissamine green staining
138 ost-AAI rAMs was studied in vivo by means of clodronate liposome-mediated depletion, adoptive transfe
139 ndent of lymphoid tissues but dependent on a clodronate liposome-sensitive population of liver-reside
140 AFIA mice had reduced CD68(+) cells, whereas clodronate liposome-treated mice had increased CD68(+) a
141 tion of these infiltrating macrophages using clodronate-liposome administration shows a significant r
142 on viral RNA abundance in the liver, whereas clodronate-liposome depletion of macrophages between day
146 rophage depletion was achieved by daily i.v. clodronate liposomes (-1 day to +3 days) during AngII in
148 onducted to determine whether treatment with clodronate liposomes (CL(2)MDP-lip), which cause depleti
149 nvestigate this, we depleted phagocytes with clodronate liposomes (CL) in vivo through systemic deliv
151 Moreover, depletion of SCS macrophages using clodronate liposomes abolished NK cell accumulation and
153 ge activation by depleting these cells using clodronate liposomes and inhibiting the inflammasome wit
154 r competence and demonstrates the utility of clodronate liposomes as an important tool in the study o
155 , depletion of salivary gland macrophages by clodronate liposomes compromised the restoration of irra
156 In addition, the treatment of rats with clodronate liposomes depleted KCs and led to increased s
159 depletion from the intratracheal delivery of clodronate liposomes enhanced Sftpc(I73T) -induced morta
160 ction, we depleted them by the inhalation of clodronate liposomes in an established mouse model of re
166 ablating liver macrophages by treatment with clodronate liposomes largely abolished the beneficial me
168 n of CD206(+) macrophages using mannosylated clodronate liposomes promoted sustained pain in Pi16(-/-
169 pletion of alveolar macrophages with inhaled clodronate liposomes reduced both NK and T cell numbers
172 y intrathecal administration of mannosylated clodronate liposomes reduced the capacity of an HDAC6 in
174 phage depletion in wild-type (WT) mice using clodronate liposomes resulted in impaired muscle regener
175 using splenectomized mice or treatment with clodronate liposomes suggested that macrophages in the s
177 apoE-/- mice before and after treatment with clodronate liposomes to deplete tissue macrophages, comp
178 effects were mitigated in mice treated with clodronate liposomes to reduce circulating monocytes and
179 monstrated by depleting the macrophages with clodronate liposomes which effectively reduced inflammat
180 peritoneal macrophages were depleted (using clodronate liposomes) from PD-1(-/-) mice, the animals'
181 epletion of macrophages in the cornea (using clodronate liposomes) prior to injury significantly inhi
182 rone mice SNF(1) mice that were treated with clodronate liposomes, but not mice treated with vehicle,
183 is in vivo, induced by the administration of clodronate liposomes, can exacerbate the autoimmune phen
185 s were not affected following treatment with clodronate liposomes, immunization of CCR2(-/-) mice, or
186 confirmed by depleting LPM with intrapleural clodronate liposomes, which abrogated the antitumoral me
187 ed for fitness and that confer resistance to clodronate liposomes, which are used to ablate immune ce
194 significantly elevated in mice treated with clodronate-liposomes at 3 and 5 days p.i., while IL-10 l
197 Both groups of inbred mice treated with clodronate-liposomes compared with PBS-liposomes (contro
199 inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathologi
200 this monocytic cell population, using either clodronate-liposomes or gadolinium chloride, prevented p
201 and selective depletion of macrophages with clodronate-liposomes protects hearts against allograft r
205 cterial plate counts in B6 mice treated with clodronate-liposomes were unchanged at 3 days and were h
206 methylene diphosphonate (Cl2MDP-liposomes or clodronate-liposomes) before priming mice with vesicular
211 xpansion was abrogated by prior injection of clodronate-loaded liposomes, indicating a role for subca
212 l amygdala mannosylated liposomes containing clodronate (m-CLD; 0 or 25 mug/side, n = 13-14/group), a
214 y of utilizing liposomal delivery means that clodronate may not be an ideal means of preventing graft
216 phoma depletion by CD20 mAb in vivo, whereas clodronate-mediated depletion of macrophages eliminated
218 modulation of the myeloid population through clodronate-mediated depletion showed a partial abrogatio
221 iven to patients with primary breast cancer, clodronate might reduce the subsequent incidence of bone
223 ype I, 97%), evaluating alendronate (n = 2), clodronate (n = 1), neridronate (n = 5), pamidronate (n
224 rrence of nonosseous metastases was similar (clodronate, n = 112; placebo, n = 128; P =.257), but the
225 uction in the occurrence of bone metastases (clodronate, n = 12; placebo, n = 28; HR, 0.44; 95% CI, 0
226 reduction in occurrence of bone metastases (clodronate, n = 63; placebo, n = 80; hazards ratio [HR],
227 re was a significant reduction in mortality (clodronate, n = 98; placebo, n = 129; P =.047) during th
229 tiinflammatory and antiresorptive effects of clodronate on macrophages and osteoclasts in vivo occur
231 ravenously with either liposome-encapsulated clodronate or empty liposomes prior to and after OBX or
232 phage depletion agent (liposome-encapsulated clodronate) or with a neutrophil depletion agent (cyclop
233 ptions recommended by the Panel include oral clodronate, oral ibandronate, and intravenous zoledronic
237 epletion of splenic macrophages by liposomal clodronate protects against PIFA-induced chemoresistance
240 se changes, whereas depleting monocytes with clodronate resulted in a modest partial inhibition.
243 r bisphosphonates, including pamidronate and clodronate, seem to be ineffective in this setting.
244 was associated with an increase in levels of clodronate-sensitive, phagocytic SiglecF(low) alveolar m
245 rom the fetal cerebral cortex with liposomal clodronate significantly increased the number of neural
247 reating mice with i.v. liposome-encapsulated clodronate, significantly attenuated perfusate cytokine
248 ocyte ablation were used: systemic liposomal clodronate (sLC), inducible depletion using CD11b diphth
250 on injury in mice pre-treated with liposomal clodronate, suggesting the process was regulated by live
252 utrophil depleting antibody (1A8), liposomal clodronate to deplete monocytes/macrophages, or PD032590
255 first time the use of liposome-encapsulated clodronate to selectively deplete macrophages during the
257 fa, Il-1beta, Il-10, Cxcl1, and iNos, in the clodronate-treated H. bilis-infected Rag2(-/-) mice comp
260 tic cells were more numerous in MAFIA versus clodronate-treated mice and flow cytometric analyses of
261 f macrophages in the OE of both sham and OBX clodronate-treated mice were significantly reduced compa
262 eta1 serum levels and pSmad3 were reduced in clodronate-treated mice, but their reductions were insuf
264 When compared with vehicle-treated controls, clodronate-treated non-lupus-prone DBF(1) mice developed
265 caspase-3 in the OE and olfactory nerves of clodronate-treated OBX mice compared to liposome-treated
268 et, vascular endothelial growth factor A, in clodronate-treated tumor cells, which correlated with re
270 , 1.32+/-0.41 mm(3) in liposome-encapsulated clodronate-treated versus 3.04+/-0.72 mm(3) in saline-tr
275 depletion of macrophages and osteoclasts via clodronate treatment had differential effects based on s
278 ion of monocytes or macrophages by liposomal clodronate treatment or genetic deficiency of macrophage
279 r, depletion of monocytes and macrophages by clodronate treatment or inhibition of gastric monocyte i
286 increase in extraction socket bone fill with clodronate was less than the large increase in trabecula
288 By depleting macrophages using liposomal clodronate, we found that alveolarization defects were s
290 iposomes containing the macrophagicidal drug clodronate were used to deplete conjunctival macrophages
291 t-generation bisphosphonates (etidronate and clodronate) were not suitable for long-term treatment an