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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.
15 is-free interval was slightly increased with clodronate (0.74, 0.55-1.00; p=0.047).
16     Patients were randomized to receive oral clodronate 1,600 mg/d or a placebo for 2 years starting
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
24                     Conversely, in mice with clodronate-ablated macrophages, neutrophils extravasate,
25       Systemic depletion of macrophages with clodronate abolished CDC-mediated cardioprotection.
26 c cells by injection of liposomes containing clodronate abolished diabetes, although inflammation rem
27              General macrophage depletion by clodronate abolished this iNKT activation.
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
30                                Both EGTA and clodronate also prevented the bisphosphonate-induced inh
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.
33        To compare the mechanism of action of clodronate and alendronate, effects on protein prenylati
34                               The effects of clodronate and AppCCl2p on bone resorption, osteoclast n
35                                              Clodronate and DTR inhibited macrophage infiltration and
36                       Two potent inhibitors, clodronate and etidronate, are already clinically approv
37                          Unlike alendronate, clodronate and its metabolite did not affect prenylation
38                 The use of mono and combined clodronate and LDD administrations may significantly red
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
55 nd could be inhibited by addition of EGTA or clodronate, both of which chelate calcium ions.
56                Pretreatment of NTN mice with clodronate but not control liposomes completely prevente
57 protocol B-34 aims to ascertain whether oral clodronate can improve outcomes in women with primary br
58                        Liposome-encapsulated clodronate caused an increase in peritoneal macrophage a
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
63       Depletion of monocytic phagocytes with clodronate completely prevented MCMV from delaying tumor
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
66         Thus, we predicted that injection of clodronate-containing liposomes (CLs), which selectively
67 rophages using subconjunctival injections of clodronate-containing liposomes before corneal infection
68                  Depletion of macrophages by clodronate-containing liposomes blocked the tumor-promot
69 normally developed spleens by treatment with clodronate-containing liposomes demonstrated that these
70                                              Clodronate-containing liposomes deplete mice of splenic
71  macrophages by intranasal administration of clodronate-containing liposomes in caspase-9 inhibitor-t
72                                    In vitro, clodronate-containing liposomes killed activated murine
73                            Mice treated with clodronate-containing liposomes show markedly less tumor
74 ed mice and compared tumor development using clodronate-containing liposomes to deplete macrophages i
75                Depletion of macrophages with clodronate-containing liposomes was also associated with
76 Treatment of PVC-211 MuLV-infected rats with clodronate-containing liposomes, which specifically kill
77 phages were depleted from ilea of mice using clodronate-containing liposomes.
78                      Our data also show that clodronate depletion of AMs leads to replenishment, but
79                                              Clodronate depletion of circulating monocytes, by contra
80                     Liposomally encapsulated clodronate (dichloromethylene diphosphonate) has previou
81 splenic phagocytic APCs by i.v. injection of clodronate- (dichloromethylene diphosphonate) containing
82 ages by intranasal instillation of liposomal clodronate diminished pneumococcal clearance.
83 which is based on intracerebral injection of clodronate disodium salt (CDS) into the PFC of adolescen
84                   The i.v. administration of clodronate effectively reduced total BALF cell numbers,
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
88  peritoneal macrophages after depletion with clodronate encapsulated liposomes.
89          Macrophage ablation by injection of clodronate-encapsulated liposomes increases blood platel
90 hamsters were treated, intratracheally, with clodronate-encapsulated liposomes or control liposomes a
91                               Treatment with clodronate-encapsulated liposomes resulted in significan
92                    Some mice were also given clodronate-encapsulated liposomes to deplete macrophages
93 nstitution of apoptosis with BH3 mimetics or clodronate-encapsulated liposomes.
94 macrophages metabolize liposome-encapsulated clodronate, following in vivo administration.
95 s or older on study entry showed benefits of clodronate for recurrence-free interval (0.75, 0.57-0.99
96 l);Pkhd1-Cre mice by treating with liposomal clodronate from postnatal day 10 until day 24.
97                                  Intravenous clodronate given after pain was established had the oppo
98                                              Clodronate, given to patients with primary operable brea
99 tion was noted in 23 of 1612 patients in the clodronate group and 12 of 1623 patients in the placebo
100 ence to treatment at 3 years was 56% for the clodronate group and 60% for the placebo group.
101 -4 diarrhoea was noted in 28 patients in the clodronate group and in ten in the placebo group.
102 not differ between groups (286 events in the clodronate group vs 312 in the placebo group; hazard rat
103 ible case of osteonecrosis of the jaw in the clodronate group.
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
106                   ZOL is preferred over oral clodronate in newly diagnosed patients with MM because o
107 e infiltration by systemic administration of clodronate-incorporated liposomes fails to suppress LSI-
108                                              Clodronate-induced depletion of the alveolar macrophage
109              Consistent with these findings, clodronate-induced macrophage depletion results in a sig
110                                 Importantly, clodronate-induced macrophage depletion significantly at
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
113 lvaria also is blocked by mevalonate whereas clodronate inhibition is not.
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
117                                              Clodronate is an alternative bisphosphonate approved wor
118 hese results provide proof-of-principle that clodronate is effective at sparing the number of donor B
119                                Additionally, clodronate is not available in the United States.
120 somiasis with macrophage-depleting liposomal clodronate (LC) to define how macrophages mediate bladde
121 n the bladder by administration of liposomal clodronate led to higher UPEC burdens.
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
124 en identifies resistance factors that impair clodronate liposome function.
125                       Interestingly, using a clodronate liposome model with targeted depletion of mat
126 nistic detail of phagolysosome formation and clodronate liposome processing.
127                                     Finally, clodronate liposome treatment in mice prevented PH in N(
128                                      Lastly, clodronate liposome treatment of TCR transgenic mice dep
129                                              Clodronate liposome treatment reduced initial liver mono
130                                              Clodronate liposome treatment significantly reduced the
131 g on day 1, which was virtually abolished by clodronate liposome treatment.
132 atment or peripheral macrophage depletion by clodronate liposome treatment.
133                  Depleting macrophages (with clodronate liposome) and neutrophils (with anti-Ly6G/1A8
134                              By day 14 after clodronate liposome, although both dural macrophages and
135 phages, through subconjunctival injection of clodronate liposome, attenuated lissamine green staining
136                                              Clodronate liposome-mediated depletion of infiltrating m
137                                              Clodronate liposome-mediated depletion of islet macropha
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
143                                              Clodronate-liposome treatment depletes circulating monoc
144                      The enhancing effect of clodronate-liposome treatment on infection (i) was shown
145                                           In clodronate-liposome-treated group, allograft hearts exhi
146 rophage depletion was achieved by daily i.v. clodronate liposomes (-1 day to +3 days) during AngII in
147       Antecedent Kupffer cell depletion with clodronate liposomes (0.5 mg/kg).
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
150                                              Clodronate liposomes (Clo-Lip) have been widely used to
151 Moreover, depletion of SCS macrophages using clodronate liposomes abolished NK cell accumulation and
152                                              Clodronate liposomes and an anti-IL-1beta antibody were
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
157                  Depletion of monocytes with clodronate liposomes during CSD recovery prevented fibri
158              Importantly, the application of clodronate liposomes effectively depleted splenic and CN
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
161             Depletion of phagocytic cells by clodronate liposomes in wild-type mice resulted in a red
162                                              Clodronate liposomes increased efferocytosis (clearance
163 th saline/WT, which was virtually ablated by clodronate liposomes independent of hypertension.
164             Intracisterna magna injection of clodronate liposomes indicated a comprehensive depletion
165                      Postnatal injections of clodronate liposomes into female RUPP and sham offspring
166 ablating liver macrophages by treatment with clodronate liposomes largely abolished the beneficial me
167 was assessed by eliminating these cells with clodronate liposomes or silica.
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
170       Depletion of peritoneal macrophages by clodronate liposomes reduced capsular fibrosis.
171        The depletion of blood monocytes with clodronate liposomes reduced neutrophil clustering in th
172 y intrathecal administration of mannosylated clodronate liposomes reduced the capacity of an HDAC6 in
173         However, Kupffer cell depletion with clodronate liposomes resulted in greater apoptosis and F
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
176       After tumors were established, we used clodronate liposomes to ablate macrophages.
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
184         By selective depletion studies using clodronate liposomes, depleting monoclonal antibodies sp
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
188 ated by alveolar macrophage depletion, using clodronate liposomes.
189 . bilis-infected Rag2(-/-) mice treated with clodronate liposomes.
190 mice that had been macrophage depleted using clodronate liposomes.
191  mice depleted of alveolar macrophages using clodronate liposomes.
192  animals after depletion of macrophages with clodronate liposomes.
193                  Depletion of macrophages by clodronate-liposomes abrogates liver EphB2 messenger RNA
194  significantly elevated in mice treated with clodronate-liposomes at 3 and 5 days p.i., while IL-10 l
195  elevated in the cornea of mice treated with clodronate-liposomes at both 3 and 5 days p.i.
196            The elimination of macrophages by clodronate-liposomes attenuated NF-kappaB-induced liver
197      Both groups of inbred mice treated with clodronate-liposomes compared with PBS-liposomes (contro
198                               Treatment with clodronate-liposomes did not affect the antigen-presenti
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
202                   Macrophage depletion using clodronate-liposomes resulted in a significant reduction
203  were determined in BALB/c mice treated with clodronate-liposomes vs control-treated mice.
204 e cornea of both groups of mice treated with clodronate-liposomes vs PBS-liposomes.
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
207 elevated in both groups of mice treated with clodronate-liposomes.
208  depleted by treating recipient animals with clodronate-liposomes.
209                              Herein, we used clodronate-loaded liposomes (CL) to locally deplete macr
210                                              Clodronate-loaded liposomes were used as a tool to deple
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
213 le of macrophages or their susceptibility to clodronate may change with time.
214 y of utilizing liposomal delivery means that clodronate may not be an ideal means of preventing graft
215                                    Moreover, clodronate-mediated cell-depletion implicated Tim4(+) re
216 phoma depletion by CD20 mAb in vivo, whereas clodronate-mediated depletion of macrophages eliminated
217                                              Clodronate-mediated depletion of phagocytic cells marked
218 modulation of the myeloid population through clodronate-mediated depletion showed a partial abrogatio
219                         At day 30, liposomal clodronate-mediated macrophage depletion reduced fibrosi
220                                    Liposomal clodronate-mediated macrophage depletion significantly r
221 iven to patients with primary breast cancer, clodronate might reduce the subsequent incidence of bone
222                     In vivo, MPhi depletion (clodronate, MPhi Fas-induced apoptosis mice) and genetic
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
228 e, risedronate, pamidronate, etidronate, and clodronate on apoptosis and signaling kinases.
229 tiinflammatory and antiresorptive effects of clodronate on macrophages and osteoclasts in vivo occur
230                  Depleting macrophages using clodronate or conditionally deleting Glul from macrophag
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
234                                    Moreover, clodronate pre-treatment increased durable donor-specifi
235                      We found that liposomal clodronate pretreatment of C57BL/6 mice permitted establ
236 asal administration of liposome-encapsulated clodronate prior to bacterial inoculation.
237 epletion of splenic macrophages by liposomal clodronate protects against PIFA-induced chemoresistance
238           Notably, the liposome-encapsulated clodronate reduced the severity of LPS-induced neurodege
239                    Macrophage depletion with clodronate reduced the tumor-infiltrating effector CD4 a
240 se changes, whereas depleting monocytes with clodronate resulted in a modest partial inhibition.
241            Macrophage depletion by liposomal clodronate resulted in a reversal of the beneficial effe
242                                          The clodronate screen identifies resistance factors that imp
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
246                                              Clodronate significantly reduced TAMs and splenic macrop
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
249                    In either case, liposomal clodronate substantially decreased RBC destruction.
250 on injury in mice pre-treated with liposomal clodronate, suggesting the process was regulated by live
251                     Thus, in AIHA, liposomal clodronate therapy may act like a temporary, medicinal s
252 utrophil depleting antibody (1A8), liposomal clodronate to deplete monocytes/macrophages, or PD032590
253                             Use of liposomal clodronate to deplete resident AMs (rAMs) resulted in in
254             Mice were treated with liposomal clodronate to investigate the effect of macrophage deple
255  first time the use of liposome-encapsulated clodronate to selectively deplete macrophages during the
256  resulting in improved survival of liposomal clodronate-treated B6 recipients.
257 fa, Il-1beta, Il-10, Cxcl1, and iNos, in the clodronate-treated H. bilis-infected Rag2(-/-) mice comp
258       Injected eyes of IFN-gamma knockout or clodronate-treated macrophage-depleted mice were examine
259                                        These clodronate-treated mice also had increased expression of
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
263 ells and TAMs, was reduced in tumor cells of clodronate-treated mice.
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
266 d in extracts from osteoclasts purified from clodronate-treated rabbits.
267 t reduction in bacterial colonization in the clodronate-treated Rag2(-/-) mice.
268 et, vascular endothelial growth factor A, in clodronate-treated tumor cells, which correlated with re
269  correlated with reduced vascular density in clodronate-treated tumors.
270 , 1.32+/-0.41 mm(3) in liposome-encapsulated clodronate-treated versus 3.04+/-0.72 mm(3) in saline-tr
271                                              Clodronate treatment affected the number of alternativel
272                                     Although clodronate treatment alone produced a peak level of bloo
273                                              Clodronate treatment also delayed the resolution of tiss
274                                  Tumors with clodronate treatment did not show decreased proliferatio
275 depletion of macrophages and osteoclasts via clodronate treatment had differential effects based on s
276                                 Furthermore, clodronate treatment hastened the onset of proteinuria a
277               In healing extraction sockets, clodronate treatment increased extraction socket trabecu
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
280       Similarly, depletion of macrophages by clodronate treatment prevented HFD-induced adipose tissu
281                    In the nonwounded tibiae, clodronate treatment significantly increased CD68+ cells
282 maxillary interseptal bone was unaffected by clodronate treatment.
283                Previous findings of adjuvant clodronate trials in different populations with operable
284                    Using phosphate, heparin, clodronate, trypan, and suramin, we demonstrate the util
285                        Liposome-encapsulated clodronate was also metabolized to AppCCl2p by rat perit
286 increase in extraction socket bone fill with clodronate was less than the large increase in trabecula
287                        Liposome-encapsulated clodronate was used to assess macrophage impact on EdCs.
288     By depleting macrophages using liposomal clodronate, we found that alveolarization defects were s
289                                      LDD and clodronate were given as a single agent or as combinatio
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
292    Therefore, we hypothesized that liposomal clodronate would be a useful agent for treating AIHA.

 
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