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Title: Teriparatide  
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Subject: Eli Lilly and Company, Bisphosphonate, ATC code H05, Osteocalcin, Sclerostin
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Clinical data
Trade names Forteo
  • C
Legal status
Routes of
Pharmacokinetic data
Bioavailability 95%
Metabolism Hepatic (nonspecific proteolysis)
Biological half-life SubQ: 1 hour
Excretion Renal (metabolites)
CAS Registry Number  Y
ATC code H05
PubChem CID:
DrugBank  Y
Chemical data
Formula C181H291N55O51S2
Molecular mass 4117.72 g/mol

Teriparatide (Forteo) Eli Lilly and Company is a recombinant form of parathyroid hormone. It is an effective anabolic (i.e., bone growing) agent[1] used in the treatment of some forms of osteoporosis.[2] It is also occasionally used off-label to speed fracture healing. Teriparatide is identical to a portion of human parathyroid hormone (PTH) and intermittent use activates osteoblasts more than osteoclasts, which leads to an overall increase in bone.


  • Medical uses 1
    • Other 1.1
    • Administration 1.2
  • Adverse effects 2
  • Mechanism of action 3
  • FDA approval 4
  • Combined teriparatide and denosumab 5
  • References 6
  • External links 7

Medical uses

Teriparatide is the only anabolic (i.e., bone growing) agent[1] indicated for use in postmenopausal women with osteoporosis at a high risk for fracture or with a history of osteoporotic fracture, patients with multiple risk factors for fracture, and for patients who have failed or are intolerant to other available osteoporosis therapy.[3] It has been FDA-approved since 2002.[4] It is effective in growing bone (e.g., 8% increase in bone density in the spine after one year)[5] and reducing the risk of fragility fractures.[4][6] Osteoporosis medications are generally safe, but some side effects of teriparatide include headache, nausea, dizziness, and limb pain.[4]

One randomized trial of postmenopausal women who had already fractured vertebra compared teriparatide at either 20 or 40 micrograms per day with placebo. After about 19 months, 14% of the women taking placebo had new vertebral fractures, as compared with 5% of the women taking 20 micrograms of teriparatide and 4% of the women taking 40 micrograms. There were also a statistically significant lower number of non-vertebral fractures in the teriparatide treated group. 20 micrograms of teriparatide increased spine and hip bone mineral density.[3]

Teriparatide is also indicated to increase bone mass in men with primary or hypogonadal osteoporosis at high risk of fracture, patients with multiple risk factors for fracture, and for patients who have failed or are intolerant to other available osteoporosis therapy.

Teriparatide is indicated as well for the treatment of men and women with osteoporosis associated with sustained systemic glucocorticoid therapy.

Teriparatide should not be prescribed for patients who are at increased risks for osteosarcoma. This includes those with Paget's Disease of bone or unexplained elevations of serum alkaline phosphate, open epiphysis, or prior radiation therapy involving the skeleton.


Teriparatide is used as off-label therapy to speed fracture repair and treat fracture nonunions.[7] It has been reported to have been successfully used to heal fracture nonunions.[8] Generally, due to HIPAA regulations, it is not publicized when American athletes receive this treatment to improve fracture recovery.[7] But an Italian soccer player, Francesco Totti, was given teriparatide after a tibia/fibula fracture, and he unexpectedly recovered in time for the 2006 World Cup.[7] It has been reported that Mark Mulder used it to recover from a hip fracture Oakland A's for the 2003 MLB playoffs[9] and Terrell Owens to recover from an ankle fracture before the 2005 Super Bowl.[9]


Teriparatide is administered by injection once a day in the thigh or abdomen.[1][3]

Adverse effects

Teriparatide has a theoretical risk of osteosarcoma, which was found in rat studies but not confirmed in humans.[1] This may be because unlike humans, rat bones grow for their entire life.[1] The tumors found in the rat studies were located on the end of the bones which grew after the injections began.[10] After nine years on the market, there were only two cases of osteosarcoma reported.[5] This risk was considered by the FDA as "extremely rare" (1 in 100,000 people)[4] and is only slightly more than the incidence in the population over 60 years old (0.4 in 100,000).[4]

Mechanism of action

Teriparatide is a portion of human parathyroid hormone (PTH), amino acid sequence 1 through 34, of the complete molecule (containing 84 amino acids). Endogenous PTH is the primary regulator of calcium and phosphate metabolism in bone and kidney. PTH increases serum calcium, partially accomplishing this by increasing bone resorption. Thus, chronically elevated PTH will deplete bone stores. However, intermittent exposure to PTH will activate osteoblasts more than osteoclasts. Thus, once-daily injections of teriparatide have a net effect of stimulating new bone formation leading to increased bone mineral density.[11][12][13]

Teriparatide is the first FDA approved agent for the treatment of osteoporosis that stimulates new bone formation.[14]

FDA approval

Teriparatide was approved by the Food and Drug Administration (FDA) on 26 November 2002, for the treatment of osteoporosis in men and postmenopausal women who are at high risk for having a fracture. The drug is also approved to increase bone mass in men with primary or hypogonadal osteoporosis who are at high risk for fracture.

Combined teriparatide and denosumab

Combined teriparatide and denosumab increased BMD more than either agent alone and more than has been reported with approved therapies. Combination treatment might, therefore, be useful to treat patients at high risk of fracture.[15]


  1. ^ a b c d e Riek AE and Towler DA (2011). "The pharmacological management of osteoporosis". Missouri Medicine 108 (2): 118–23.  
  2. ^ Saag KG, Shane E, Boonen S, et al. (November 2007). "Teriparatide or alendronate in glucocorticoid-induced osteoporosis". The New England Journal of Medicine 357 (20): 2028–39.  
  3. ^ a b c Estébanez, P.; Sarasqueta, C.; Nájera, R.; Contreras, G.; Pérez, L.; Fitch, K.; Vicente, A. (1992). "Prevalence of HIV-1, HIV-2, and HTLV-I/II in Spanish seamen". Journal of acquired immune deficiency syndromes 5 (3): 316–317.  
  4. ^ a b c d e Rizzoli, R.; Reginster, J. Y.; Boonen, S.; Bréart, G. R.; Diez-Perez, A.; Felsenberg, D.; Kaufman, J. M.; Kanis, J. A.; Cooper, C. (2011). "Adverse Reactions and Drug–Drug Interactions in the Management of Women with Postmenopausal Osteoporosis". Calcified Tissue International 89 (2): 91–104.  
  5. ^ a b Kawai, M.; Mödder, U. I.; Khosla, S.; Rosen, C. J. (2011). "Emerging therapeutic opportunities for skeletal restoration". Nature Reviews Drug Discovery 10 (2): 141–156.  
  6. ^ Murad, M. H.; Drake, M. T.; Mullan, R. J.; Mauck, K. F.; Stuart, L. M.; Lane, M. A.; Abu Elnour, N. O.; Erwin, P. J.; Hazem, A.; Puhan, M. A.; Li, T.; Montori, V. M. (2012). "Comparative Effectiveness of Drug Treatments to Prevent Fragility Fractures: A Systematic Review and Network Meta-Analysis". Journal of Clinical Endocrinology & Metabolism 97 (6): 1871–1880.  
  7. ^ a b c Bruce Jancin (2011-12-12). "Accelerating Fracture Healing With Teriparatide". Internal Medicine News Digital Network. Retrieved 2013-09-20. 
  8. ^ Giannotti, S.; Bottai, V.; Dell’Osso, G.; Pini, E.; De Paola, G.; Bugelli, G.; Guido, G. (2013). "Current medical treatment strategies concerning fracture healing". Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases 10 (2): 116–120.  
  9. ^ a b William L. Carroll (2005). "Chapter 1: Defining the Issue". The Juice: The Real Story of Baseball's Drug Problems.  
  10. ^
  11. ^ Bauer E, Aub JC, Albright F. Studies of calcium and phosphorus metabolism: V. Study of the bone trabeculae as a readily available reserve supply of calcium. J Exp Med. 1929;49:145-162.
  12. ^ Selye H. On the stimulation of new bone formation with parathyroid extract and irradiated ergosterol. Endocrinology. 1932;16:547-558.
  13. ^ Dempster, D. W.; Cosman, F.; Parisien, M.; Shen, V.; Lindsay, R. (1993). "Anabolic actions of parathyroid hormone on bone". Endocrine reviews 14 (6): 690–709.  
  14. ^ Fortéo: teriparatide (rDNA origin) injection
  15. ^ Joy N Tsai MD,Alexander V Uihlein MD,Hang Lee PhD,Ruchit Kumbhani BA,Erica Siwila-Sackman BA,Elizabeth A McKay BA,Sherri-Ann M Burnett-Bowie MD,Robert M Neer MD,Dr Benjamin Z Leder MD. Teriparatide and denosumab, alone or combined, in women with postmenopausal osteoporosis: the DATA study randomised trial. The Lancet - 15 May 2013 doi:10.1016/S0140-6736(13)60856-9

External links

  • Teriparatide at National Institutes of Health.
  • When to Use Teriparatide - Medscape.
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