PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 21942989-9 2011 Intravenous ferric carboxymaltose improved mean Hb, serum ferritin, and transferrin saturation levels; the mean end-of-trial increase over oral iron was, for Hb 4.8 (95% confidence interval 3.3 to 6.3) g/L, for ferritin 163 (153 to 173) mug/L, and for transferrin saturation 5.3% (3.7 to 6.8%). ferric carboxymaltose 12-33 transferrin Homo sapiens 72-83 21942989-9 2011 Intravenous ferric carboxymaltose improved mean Hb, serum ferritin, and transferrin saturation levels; the mean end-of-trial increase over oral iron was, for Hb 4.8 (95% confidence interval 3.3 to 6.3) g/L, for ferritin 163 (153 to 173) mug/L, and for transferrin saturation 5.3% (3.7 to 6.8%). ferric carboxymaltose 12-33 transferrin Homo sapiens 252-263 34854600-8 2021 CONCLUSION: FCM injections may cause FGF23 mediated hypophosphatemia already 4 weeks after suppletion. ferric carboxymaltose 12-15 fibroblast growth factor 23 Homo sapiens 37-42 20648930-10 2010 Treatment with FCM improved indices of anemia (hemoglobin [Hb], ferritin and transferrin saturation [TSAT] values). ferric carboxymaltose 15-18 transferrin Homo sapiens 77-88 19405553-6 2009 Ferric carboxymaltose is a macromolecular ferric hydroxide carbohydrate complex, which allows for controlled delivery of iron within the cells of the reticuloendothelial system and subsequent delivery to the iron-binding proteins ferritin and transferrin, with minimal risk of release of large amounts of ionic iron in the serum. ferric carboxymaltose 0-21 transferrin Homo sapiens 243-254 19405553-7 2009 Intravenous administration of ferric carboxymaltose results in transient elevations in serum iron, serum ferritin and transferrin saturation, and, ultimately, in the correction of haemoglobin levels and replenishment of depleted iron stores. ferric carboxymaltose 30-51 transferrin Homo sapiens 118-129 19405553-21 2009 Recipients of ferric carboxymaltose demonstrated improvements from baseline in serum ferritin levels and transferrin saturation, as well as improvements from baseline in HR-QOL assessment scores. ferric carboxymaltose 14-35 transferrin Homo sapiens 105-116 19405553-22 2009 Ferric carboxymaltose was at least as effective as ferrous sulfate with regard to endpoints related to serum ferritin levels, transferrin saturation and HR-QOL. ferric carboxymaltose 0-21 transferrin Homo sapiens 126-137 34470831-9 2021 Proportional changes from baseline to week 40 differed by -31% (98.3% CI: -52 to -0.1) for ferritin, by 1% (98.3% CI: -7 to 10) for transferrin and by -27% (98.3% CI: -39 to -13) for transferrin saturation in the ferric carboxymaltose compared to the iron sucrose arm. ferric carboxymaltose 213-234 transferrin Homo sapiens 183-194 34007138-14 2021 CONCLUSION: Fibroblast growth factor 23 has a key role in FCM induced hypophosphatemia, probably by inducing loss of phosphate in the urine. ferric carboxymaltose 58-61 fibroblast growth factor 23 Homo sapiens 12-39 34079413-9 2021 All 10 studies reported statistically greater changes in hemoglobin concentration, serum ferritin, and/or transferrin saturation with FCM treatment compared with comparators (placebo, oral iron, standard care, or a combination of these). ferric carboxymaltose 134-137 transferrin Homo sapiens 106-117 33962799-11 2021 However, the mechanism of ferric carboxymaltose- induced increase in intact FGF-23 is still unknown. ferric carboxymaltose 26-47 fibroblast growth factor 23 Homo sapiens 76-82 33910844-9 2021 CONCLUSION: Patients who received FCM reached satisfactory values of transferrin saturation and ferritin, presented fewer coronary artery events and cardiovascular events, and could reduce doses of ESA. ferric carboxymaltose 34-37 transferrin Homo sapiens 69-80 33918110-7 2021 Ferritin, iron and transferrin saturation levels were significantly higher in the FCM group from 2 to 12 weeks postoperatively (all p < 0.05). ferric carboxymaltose 82-85 transferrin Homo sapiens 19-30 33230080-17 2021 CONCLUSION: FCM appears to be effective in correcting IDA in children across a wide range of GI indications and all ages. ferric carboxymaltose 12-15 G protein subunit alpha i1 Homo sapiens 93-95 32154642-6 2020 Six months of FCM IV treatment once a week increased ferritin and Hb compared to sodium ferric gluconate once a week leading to decreased erythropoietin consumption from 24 000 to 15 000 U/patient/week with an erythropoietin annual expense reduction. ferric carboxymaltose 14-17 erythropoietin Homo sapiens 138-152 32730929-2 2020 However, administration of FCM increases intact levels of fibroblast growth factor 23 (FGF23), which causes hypophosphatemia due to renal phosphate wasting, calcitriol deficiency and secondary hyperparathyroidism. ferric carboxymaltose 27-30 fibroblast growth factor 23 Homo sapiens 58-85 32730929-2 2020 However, administration of FCM increases intact levels of fibroblast growth factor 23 (FGF23), which causes hypophosphatemia due to renal phosphate wasting, calcitriol deficiency and secondary hyperparathyroidism. ferric carboxymaltose 27-30 fibroblast growth factor 23 Homo sapiens 87-92 32730929-7 2020 We hypothesized that FCM would decrease phosphate, increase intact FGF23 (iFGF23), and decrease c-terminal FGF23 (cFGF23). ferric carboxymaltose 21-24 fibroblast growth factor 23 Homo sapiens 67-72 32730929-7 2020 We hypothesized that FCM would decrease phosphate, increase intact FGF23 (iFGF23), and decrease c-terminal FGF23 (cFGF23). ferric carboxymaltose 21-24 fibroblast growth factor 23 Homo sapiens 75-80 32154642-6 2020 Six months of FCM IV treatment once a week increased ferritin and Hb compared to sodium ferric gluconate once a week leading to decreased erythropoietin consumption from 24 000 to 15 000 U/patient/week with an erythropoietin annual expense reduction. ferric carboxymaltose 14-17 erythropoietin Homo sapiens 210-224 32154642-8 2020 The FCM IV administration protocol for our HD-CAL patients was safe and no adverse events were reported, resulting in significantly increased ferritin, transferrin saturation, and Hb levels, reduction of erythropoietin requirements, and consequently reduction of erythropoietin expenses. ferric carboxymaltose 4-7 transferrin Homo sapiens 152-163 32154642-8 2020 The FCM IV administration protocol for our HD-CAL patients was safe and no adverse events were reported, resulting in significantly increased ferritin, transferrin saturation, and Hb levels, reduction of erythropoietin requirements, and consequently reduction of erythropoietin expenses. ferric carboxymaltose 4-7 erythropoietin Homo sapiens 204-218 32154642-8 2020 The FCM IV administration protocol for our HD-CAL patients was safe and no adverse events were reported, resulting in significantly increased ferritin, transferrin saturation, and Hb levels, reduction of erythropoietin requirements, and consequently reduction of erythropoietin expenses. ferric carboxymaltose 4-7 erythropoietin Homo sapiens 263-277 32839355-0 2020 Ferric carboxymaltose versus ferric gluconate in hemodialysis patients: Reduction of erythropoietin dose in 4 years of follow-up. ferric carboxymaltose 0-21 erythropoietin Homo sapiens 85-99 33040491-8 2020 FCM was also associated with a significant and early improvement in RVEF at 7 days (RVSD1 : Delta6.9%, P = 0.003; RVSD2 : Delta3.2%, P = 0.003) that persisted at 30 days (RVSD1 : Delta8.1%, P < 0.001; RVSD2 : Delta4.7%, P < 0.001). ferric carboxymaltose 0-3 delta like canonical Notch ligand 3 Homo sapiens 122-128 33040491-8 2020 FCM was also associated with a significant and early improvement in RVEF at 7 days (RVSD1 : Delta6.9%, P = 0.003; RVSD2 : Delta3.2%, P = 0.003) that persisted at 30 days (RVSD1 : Delta8.1%, P < 0.001; RVSD2 : Delta4.7%, P < 0.001). ferric carboxymaltose 0-3 delta like canonical Notch ligand 4 Homo sapiens 209-215 32839355-6 2020 Results: FCM increased transferrin saturation (TSAT) levels by 11.9% (P < 0.001) with respect to FX. ferric carboxymaltose 9-12 transferrin Homo sapiens 23-34 32839355-8 2020 The monthly dose of EPO was reduced in the FCM period (-6,404.1 international unit [IU]; 95% confidence interval, -10,643.5 IU; -2,164.6 IU; P = 0.003), as well as the erythropoietin resistance index (P = 0.004). ferric carboxymaltose 43-46 erythropoietin Homo sapiens 20-23 32839355-8 2020 The monthly dose of EPO was reduced in the FCM period (-6,404.1 international unit [IU]; 95% confidence interval, -10,643.5 IU; -2,164.6 IU; P = 0.003), as well as the erythropoietin resistance index (P = 0.004). ferric carboxymaltose 43-46 erythropoietin Homo sapiens 168-182 32839355-9 2020 During the period with FCM, ferritin levels were higher than during FX (P < 0.001), while transferrin was reduced (P = 0.001). ferric carboxymaltose 23-26 transferrin Homo sapiens 90-101 32839355-10 2020 Conclusion: During FCM treatment, minor doses of EPO were administered if compared to those delivered during FX therapy. ferric carboxymaltose 19-22 erythropoietin Homo sapiens 49-52 32654663-7 2020 Within 24 h after iron supplementation, women in the FCM group had significant higher plasma intact FGF23 (p < 0.001) and lower plasma 1.25-dihydroxyvitamin D (p < 0.001). ferric carboxymaltose 53-56 fibroblast growth factor 23 Homo sapiens 100-105 32444112-11 2020 An emerging complication affecting 50-74% of patients treated with ferric carboxymaltose in prospective clinical trials is hypophosphatemia - or more accurately the 6H syndrome (hyperphosphaturic hypophosphatemia triggered by high fibroblast growth factor 23 that causes hypovitaminosis D, hypocalcemia and secondary hyperparathyroidism). ferric carboxymaltose 67-88 fibroblast growth factor 23 Homo sapiens 231-258 32923530-2 2020 Laboratory study confirmed fibroblast growth factor 23 (FGF-23)-mediated hypophosphatemia as the main cause of a severe osteomalacia induced by ferric carboxymaltose (FCM).After 3 months or oral phosphate replacement and switching to iron sucrose, serum phosphate levels were normalized and patient improved clinically. ferric carboxymaltose 144-165 fibroblast growth factor 23 Homo sapiens 27-54 32923530-2 2020 Laboratory study confirmed fibroblast growth factor 23 (FGF-23)-mediated hypophosphatemia as the main cause of a severe osteomalacia induced by ferric carboxymaltose (FCM).After 3 months or oral phosphate replacement and switching to iron sucrose, serum phosphate levels were normalized and patient improved clinically. ferric carboxymaltose 144-165 fibroblast growth factor 23 Homo sapiens 56-62 32923530-2 2020 Laboratory study confirmed fibroblast growth factor 23 (FGF-23)-mediated hypophosphatemia as the main cause of a severe osteomalacia induced by ferric carboxymaltose (FCM).After 3 months or oral phosphate replacement and switching to iron sucrose, serum phosphate levels were normalized and patient improved clinically. ferric carboxymaltose 167-170 fibroblast growth factor 23 Homo sapiens 56-62 31937462-10 2020 Iron-binding capacity was transiently well utilized after dosing, as indicated by transferrin saturation >88% with 500-mg FCM and >90% with 1000-mg FCM. ferric carboxymaltose 122-125 transferrin Homo sapiens 82-93 32221822-11 2020 CONCLUSION: Patients with previous bariatric surgery receiving FCM are at considerable risk of developing significant hypophosphatemia secondary to increased renal phosphate wasting through a mechanism involving FGF23. ferric carboxymaltose 63-66 fibroblast growth factor 23 Homo sapiens 212-217 32295216-8 2020 In Vk*MYC mice, addition of iron dextran or ferric carboxymaltose to the bortezomib-melphalan-prednisone (VMP) regimen increased the therapeutic response and prolonged remission without causing evident toxicity. ferric carboxymaltose 44-65 neurensin 1 Mus musculus 106-109 33261258-0 2020 Effect of intravenous ferric carboxymaltose supplementation in non-anaemic iron deficient patients undergoing hip and knee arthroplasty. ferric carboxymaltose 22-43 hedgehog interacting protein Homo sapiens 110-113 31483921-4 2020 With some types of iron formulation (especially iron carboxymaltose) a particular side-effect has been observed: hypophosphatemia, mediated by FGF23. ferric carboxymaltose 48-67 fibroblast growth factor 23 Homo sapiens 143-148 31519999-5 2020 The balance between FGF23 production, post-translational modification and cleavage is maintained or perturbed in different hereditary monogenic conditions and in acquired conditions that mimic these genetic disorders, including iron deficiency, inflammation, treatment with ferric carboxymaltose and chronic kidney disease. ferric carboxymaltose 274-295 fibroblast growth factor 23 Homo sapiens 20-25 31928094-5 2020 Odds ratios of any serious or severe HSR (all groups) with FDI relative to FCM were 0.41, 0.39, and 0.45 according to the Bayesian, naive and adjusted approaches, respectively.Conclusions: The risk of serious or severe HSRs was lower with FDI relative to FCM and IS. ferric carboxymaltose 75-78 HSR Homo sapiens 37-40 31928094-5 2020 Odds ratios of any serious or severe HSR (all groups) with FDI relative to FCM were 0.41, 0.39, and 0.45 according to the Bayesian, naive and adjusted approaches, respectively.Conclusions: The risk of serious or severe HSRs was lower with FDI relative to FCM and IS. ferric carboxymaltose 255-258 HSR Homo sapiens 37-40 31561177-9 2020 Postoperative serum ferritin and transferrin saturation were also higher in the ferric carboxymaltose group (MD, 373.85 mug/L; 95% CI, 298.13 to 449.56; P < 0.00001; MD, 10.35%; 95% CI, 4.59 to 16.10; P < 0.00001, respectively). ferric carboxymaltose 80-101 transferrin Homo sapiens 33-44 31489572-8 2019 In addition, other clinical parameters (ferritin, transferrin saturation, erythropoietin resistance index) improved after switching from FG to FCM. ferric carboxymaltose 143-146 erythropoietin Homo sapiens 74-88 31197861-7 2019 At Day 42, normalisation of transferrin saturation to 25% or greater was observed in 76.9% of FCM vs 24.1% of FeSulf-treated patients (P < 0.001). ferric carboxymaltose 94-97 transferrin Homo sapiens 28-39 30074935-10 2018 CONCLUSIONS: After preoperative administration of erythropoietin, body iron stores and stimulation of the erythropoiesis were greater with intravenous ferric carboxymaltose than with oral ferrous sulfate supplementation. ferric carboxymaltose 151-172 erythropoietin Homo sapiens 50-64 30518682-5 2018 Ferric carboxymaltose, but not ferumoxytol, increased circulating concentrations of biologically active FGF23 (mean within-patient percentage change from baseline to week 2 peak: +302.8 +- 326.2% vs. +10.1 +- 61.0%; P < 0.001), which was significantly associated with contemporaneous hypophosphatemia, renal phosphate wasting, and decreased serum calcitriol and calcium, and increased PTH concentrations. ferric carboxymaltose 0-21 fibroblast growth factor 23 Homo sapiens 104-109 30518682-6 2018 CONCLUSIONS: Ferric carboxymaltose rapidly increases biologically active FGF23 in patients with iron deficiency anemia. ferric carboxymaltose 13-34 fibroblast growth factor 23 Homo sapiens 73-78 30518682-7 2018 Paralleling hereditary and other acquired syndromes of hypophosphatemic rickets/osteomalacia, ferric carboxymaltose-induced FGF23 elevation triggers a pathophysiological cascade of renal phosphate wasting, calcitriol deficiency, and secondary hyperparathyroidism that frequently culminates in hypophosphatemia. ferric carboxymaltose 94-115 fibroblast growth factor 23 Homo sapiens 124-129 29298794-0 2018 Severe FGF23-based hypophosphataemic osteomalacia due to ferric carboxymaltose administration. ferric carboxymaltose 57-78 fibroblast growth factor 23 Homo sapiens 7-12 29298794-2 2018 FCM administration can cause an asymptomatic hypophosphataemia secondary to fibroblast growth factor 23 (FGF23) dysregulation. ferric carboxymaltose 0-3 fibroblast growth factor 23 Homo sapiens 76-103 29298794-2 2018 FCM administration can cause an asymptomatic hypophosphataemia secondary to fibroblast growth factor 23 (FGF23) dysregulation. ferric carboxymaltose 0-3 fibroblast growth factor 23 Homo sapiens 105-110 29298794-5 2018 We report a case of a patient with Crohn"s disease and chronic iron-deficiency anaemia receiving multiple doses of FCM who developed severe hypophosphataemic osteomalacia with urinary phosphate loss and increased FGF23. ferric carboxymaltose 115-118 fibroblast growth factor 23 Homo sapiens 213-218 29298794-6 2018 FGF23 excess and osteomalacia resolved only months after FCM discontinuation and aggressive phosphate repletion. ferric carboxymaltose 57-60 fibroblast growth factor 23 Homo sapiens 0-5 27545647-11 2017 Intravenous injection of ferric carboxymaltose replenished cardiac iron stores, restored mitochondrial respiratory capacity and inotropic reserve, and attenuated adverse remodelling after myocardial infarction in Irp-targeted mice but not in control mice. ferric carboxymaltose 25-46 wingless-type MMTV integration site family, member 2 Mus musculus 213-216 27278921-0 2017 Ferric carboxymaltose vs. oral iron in the treatment of pregnant women with iron deficiency anemia: an international, open-label, randomized controlled trial (FER-ASAP). ferric carboxymaltose 0-21 microtubule associated protein 9 Homo sapiens 163-167 28701470-11 2017 FCM significantly increased serum ferritin and transferrin saturation. ferric carboxymaltose 0-3 transferrin Homo sapiens 47-58 28276325-9 2017 RESULTS: In the two index patients an increase in FGF-23 and a decrease in phosphate concentrations were observed after FCM administration. ferric carboxymaltose 120-123 fibroblast growth factor 23 Homo sapiens 50-56 28095881-5 2017 The pre-specified endpoint of mean (SE) change in eGFR from baseline to month 12 was +0.7 (0.9) mL/min/1.73 m2 with high ferritin FCM (p = 0.15 versus oral iron), -0.9 (0.9) mL/min/1.73 m2 with low ferritin FCM (p = 0.99 versus oral iron) and -0.9 (0.7) mL/min/1.73 m2 with oral iron. ferric carboxymaltose 130-133 epidermal growth factor receptor Homo sapiens 50-54 27907058-14 2016 A significant increase in the phosphaturic hormone intact FGF-23 in hypophosphatemic patients shows that this adverse event is caused by FCM-induced hormone dysregulation. ferric carboxymaltose 137-140 fibroblast growth factor 23 Homo sapiens 58-64 27852236-10 2016 Both serum ferritin (p < 0.001) and hepcidin (p < 0.001) increased in both groups, and the increase in hepcidin was greater in the FCM group (p = 0.03 for between-group difference). ferric carboxymaltose 137-140 hepcidin antimicrobial peptide Homo sapiens 109-117 27282576-0 2016 Assessment of serum bioactive hepcidin-25, soluble transferrin receptor and their ratio in predialysis patients: Correlation with the response to intravenous ferric carboxymaltose. ferric carboxymaltose 158-179 hepcidin antimicrobial peptide Homo sapiens 30-38 27282576-0 2016 Assessment of serum bioactive hepcidin-25, soluble transferrin receptor and their ratio in predialysis patients: Correlation with the response to intravenous ferric carboxymaltose. ferric carboxymaltose 158-179 transferrin Homo sapiens 51-62 27282576-9 2016 CONCLUSIONS: These results suggest that lower Hepcidin-25, as well as higher sTfR and sTfR/Hepcidin-25 ratio were significant predictors of favorable hemoglobin response within a month after IV administration of FCM in patients with CKD. ferric carboxymaltose 212-215 hepcidin antimicrobial peptide Homo sapiens 91-99 27276035-6 2016 The increase in hepcidin from baseline was significantly smaller with low ferritin FCM or oral iron vs high ferritin FCM at all time points up to week 52. ferric carboxymaltose 83-86 hepcidin antimicrobial peptide Homo sapiens 16-24 27276035-6 2016 The increase in hepcidin from baseline was significantly smaller with low ferritin FCM or oral iron vs high ferritin FCM at all time points up to week 52. ferric carboxymaltose 117-120 hepcidin antimicrobial peptide Homo sapiens 16-24 26816915-8 2015 RESULTS: Ferric carboxymaltose similar resulted in deranged iron distribution versus iron sucrose originator as indicated by increased serum iron, transferrin saturation and tissue iron(III) deposits as well as decreased ferritin deposits in the liver, heart and kidneys versus iron sucrose originator. ferric carboxymaltose 9-30 transferrin Rattus norvegicus 147-158 25683972-8 2015 Compared with placebo, treatment with FCM was associated with an increase in eGFR [treatment effect: week 4, 2.11 +- 1.21 (P = 0.082); week 12, 2.41 +- 1.33 (P = 0.070); and week 24, 2.98 +- 1.44 mL/min/1.73 m(2) (P = 0.039)]. ferric carboxymaltose 38-41 CD59 molecule (CD59 blood group) Homo sapiens 199-204 25973894-13 2015 Exposure to ferric carboxymaltose and iron dextran resulted in release of tumor necrosis factor alpha. ferric carboxymaltose 12-33 tumor necrosis factor Homo sapiens 74-101 24688754-11 2014 Mechanistic studies demonstrated that the transient, asymptomatic reduction in serum phosphate observed following FCM administration results from induction of fibroblast growth factor 23, which in turn induces renal phosphate excretion. ferric carboxymaltose 114-117 fibroblast growth factor 23 Homo sapiens 159-186 25326244-6 2015 IS and FCM were non-toxic for HepG2-cells and THP-1 macrophages were more sensitive to FCM compared to IS at all concentrations tested. ferric carboxymaltose 87-90 GLI family zinc finger 2 Homo sapiens 46-51 25326244-9 2015 Effect of vitamin C on mobilisation to transferrin was an increase with IS and interestingly a decrease with FCM. ferric carboxymaltose 109-112 transferrin Homo sapiens 39-50 25326244-11 2015 Ascorbic acid reduces transferrin-chelatable iron from ferric carboxymaltose, thus effects on hepcidin expression should be investigated in clinical studies. ferric carboxymaltose 55-76 transferrin Homo sapiens 22-33 24688754-12 2014 An elevated hepcidin level may identify patients with IDA who will not respond to oral iron but will respond to FCM. ferric carboxymaltose 112-115 hepcidin antimicrobial peptide Homo sapiens 12-20 24373521-5 2013 Therefore, the effect of a single high iv dose of two different iron preparations, iron isomaltoside 1000 (IIM) and ferric carboxymaltose (FCM), on plasma levels of FGF23 and phosphate was examined in normal and uremic iron repleted rats. ferric carboxymaltose 116-137 fibroblast growth factor 23 Rattus norvegicus 165-170 24373521-5 2013 Therefore, the effect of a single high iv dose of two different iron preparations, iron isomaltoside 1000 (IIM) and ferric carboxymaltose (FCM), on plasma levels of FGF23 and phosphate was examined in normal and uremic iron repleted rats. ferric carboxymaltose 139-142 fibroblast growth factor 23 Rattus norvegicus 165-170 23902731-0 2013 Effect of ferric carboxymaltose on serum phosphate and C-terminal FGF23 levels in non-dialysis chronic kidney disease patients: post-hoc analysis of a prospective study. ferric carboxymaltose 10-31 fibroblast growth factor 23 Homo sapiens 66-71 23902731-13 2013 FCM causes a significant decrease in FGF23 levels without changes to other bone metabolism parameters. ferric carboxymaltose 0-3 fibroblast growth factor 23 Homo sapiens 37-42 23078888-10 2013 Markers of body levels of iron increased or remained at normal levels in subjects given FCM (ferritin increased by 30.3 mug/L, transferrin saturation increased by 0.6%) but decreased in the group given placebo (ferritin decreased by 36.1 mug/L, transferrin saturation decreased by 4.0%). ferric carboxymaltose 88-91 transferrin Homo sapiens 127-138 23078888-10 2013 Markers of body levels of iron increased or remained at normal levels in subjects given FCM (ferritin increased by 30.3 mug/L, transferrin saturation increased by 0.6%) but decreased in the group given placebo (ferritin decreased by 36.1 mug/L, transferrin saturation decreased by 4.0%). ferric carboxymaltose 88-91 transferrin Homo sapiens 245-256 23071262-9 2013 Also patients with ferritin >500 ng/ml but low transferrin saturation benefited from FCM treatment. ferric carboxymaltose 88-91 transferrin Homo sapiens 50-61