Profile of romosozumab and its potential in the management of osteoporosis.

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Term Occurence Count Dictionary
osteoporosis 27 endocrinologydiseases
raloxifene 1 endocrinologydiseasesdrugs
vascular calcification 2 endocrinologydiseases
Denosumab 1 endocrinologydiseasesdrugs
Teriparatide 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Denosumab 35665 2015;75(10):1049–1058[36] which was originally sourced from Leder BZ, Tsai JN, Uihlein AV, et al, Two years of Denosumab and teriparatide administration in postmenopausal women with osteoporosis (The DATA Extension Study):
Teriparatide 23268 open-label, international multicenter STRUCTURE study (STudy evaluating effect of RomosozUmab Compared with Teriparatide in postmenopaUsal women with osteoporosis at high risk for fracture pReviously treated with bisphosphonatE
raloxifene 2326 mortality.[1],[2] Several medications have been developed to treat osteoporosis, including estrogen, raloxifene , bisphosphonates, denosumab, and teriparatide. All of these medications are antiresorptive agents except
Select Disease Character Offset Disease Term Instance
osteoporosis 105 Title: Drug Design, Development and TherapyProfile of romosozumab and its potential in the management of osteoporosis Sian Yik LimMarcy B Bolster1Straub Bone & Joint Center, Straub Medical Center, Honolulu, HI2Division
osteoporosis 1832 Romosozumab holds significant potential, by a novel mechanism of action, to expand our ability to treat osteoporosis . More studies are needed to determine the ideal setting in which romosozumab may be used to optimize
osteoporosis 1946 More studies are needed to determine the ideal setting in which romosozumab may be used to optimize osteoporosis treatment.GraphicalVideo abstractIntroductionOsteoporosis is a skeletal disorder in which bone strength
osteoporosis 2292 health care cost, morbidity, and mortality.[1],[2] Several medications have been developed to treat osteoporosis , including estrogen, raloxifene, bisphosphonates, denosumab, and teriparatide. All of these medications
osteoporosis 2566 osteoanabolic medications is needed for a more effective, individualized, and targeted approach in osteoporosis treatment.[3] Other anabolic medications, including abaloparatide (Radius Health, Inc., Waltham, MA,
osteoporosis 2862 under development. In this article, we discuss the profile of romosozumab and its potential role in osteoporosis treatment.The Wnt signaling pathway and bone healthThe term “Wnt” originates from the acronym between
osteoporosis 5861 reduced bone mass, skeletal deformities, and fragility fractures during childhood, a condition known as osteoporosis –pseudoglioma syndrome.[10]SclerostinSclerostin is a glycoprotein produced by osteocytes. The SOST
osteoporosis 7516 and therefore bone formation.[11],[17] The former mechanism may have relevance in the pathogenesis of osteoporosis of disuse where prolonged immobility leads to decreased bone mass.[6]Distinguishing genetic alterations
osteoporosis 7784 sclerostin have helped to recognize the important role that sclerostin inhibition could have in treating osteoporosis . Clues to the possible utility of inhibiting sclerostin in the treatment of osteoporosis came from two
osteoporosis 7873 in treating osteoporosis. Clues to the possible utility of inhibiting sclerostin in the treatment of osteoporosis came from two rare autosomal recessive genetic conditions of sclerosteosis and van Buchem’s disease.
osteoporosis 9789 that inhibits sclerostin (a Wnt pathway inhibitor) as a way to increase bone mass and likewise treat osteoporosis (Figure 2).[7],[23]Antisclerostin antibodies in animal studiesSeveral animal models have shown the effect
osteoporosis 19010 Phase I studies led to Phase II studies evaluating the efficacy of romosozumab for the treatment of osteoporosis .[28],[29]Phase II trials: efficacy and safety of romosozumabA Phase II randomized, placebo-controlled,
osteoporosis 23310 study (STudy evaluating effect of RomosozUmab Compared with Teriparatide in postmenopaUsal women with osteoporosis at high risk for fracture pReviously treated with bisphosphonatE therapy).[38] This study aimed to assess
osteoporosis 23611 after bisphosphonate treatment. The study included 436 postmenopausal women aged 55–85 years with osteoporosis (T-score ≤−2.5 at the lumbar spine, femoral neck, or total hip) who had taken an oral bisphosphonate
osteoporosis 25215 there are two large Phase III fracture studies exploring the utility of romosozumab in the treatment of osteoporosis . The first study (ClinicalTrial.gov identifier: NCT01631214) compares romosozumab in the first year
osteoporosis 31092 warranted.Future directionsRomosozumab holds significant potential to enhance our ability to treat osteoporosis in the future. Due to its potency as an osteoanabolic agent, romosozumab should be an excellent treatment
osteoporosis 31243 an osteoanabolic agent, romosozumab should be an excellent treatment option for patients with severe osteoporosis . With better ability to increase BMD at both the hip and the spine, romosozumab may help clinicians
osteoporosis 31402 the hip and the spine, romosozumab may help clinicians to adopt a “treat to target” approach for osteoporosis in the future.[46] There have been encouraging results of the utility of sclerostin antibodies in glucocorticoid-induced
osteoporosis 31536 There have been encouraging results of the utility of sclerostin antibodies in glucocorticoid-induced osteoporosis , immobilization-induced bone loss, chronic inflammation-induced bone loss, type 2 diabetes bone loss,
osteoporosis 33077 potent bone anabolic agents to date and holds significant potential to increase our ability to treat osteoporosis in the future. Further studies are needed to confirm its safety profile and to evaluate ways to optimize
osteoporosis 33247 safety profile and to evaluate ways to optimize the use of this potent bone anabolic agent to treat osteoporosis .Figure 1The canonical Wnt-β-catenin signaling pathway and the effects of inhibition through loss of
osteoporosis 34382 AD, Shoback D, Lewiecki EM. Sclerostin inhibition: a novel therapeutic approach in the treatment of osteoporosis . Int J Womens Health. 2015;7:565–580.[7]Abbreviation: LRP, LDL-receptor-related protein.Figure 2Mechanism
osteoporosis 35087 AD, Shoback D, Lewiecki EM. Sclerostin inhibition: a novel therapeutic approach in the treatment of osteoporosis . Int J Womens Health. 2015;7:565–580.[7]Abbreviation: LRP, LDL-receptor-related protein.Figure 3Changes
osteoporosis 35531 Modulating bone resorption and bone formation in opposite directions in the treatment of postmenopausal osteoporosis . Drugs. 2015;75(10):1049–1058[36] which was originally sourced from Leder BZ, Tsai JN, Uihlein AV,
osteoporosis 35736 Uihlein AV, et al, Two years of Denosumab and teriparatide administration in postmenopausal women with osteoporosis (The DATA Extension Study): a randomized controlled trial, J Clin Endocrinol Metab, 2014;99(5):1694–1700,
osteoporosis 39415 teriparatide (7.1% BMD increase)NCT01575834Registrational study with AMG 785 to treat postmenopausal osteoporosis Phase III study7,180 postmenopausal women, with osteoporosis (T-score of −2.5 to −3.5 at the total
osteoporosis 39476 study with AMG 785 to treat postmenopausal osteoporosis Phase III study7,180 postmenopausal women, with osteoporosis (T-score of −2.5 to −3.5 at the total hip or femoral neck) Patients randomized to receive romosozumab
vascular calcification 30391 calcification. The sclerostin expression may represent a counter-regulatory mechanism aimed at suppressing vascular calcification progression. However, more studies are needed to clarify this hypothesis.[44] Notably, patients with
vascular calcification 30697 risk for cardiovascular disease.[45] Furthermore, SOST-knockout mice have not been noted to develop vascular calcification .[45] In the aforementioned Phase III trial, cardiovascular events were balanced between the romosozumab

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