| Denosumab |
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PHYTONUTRIENTS AND DRUG PRODUCTS. THIS WEBSITE ALSO TALKS ABOUT SOME POPULAR HEALTH ISSUES AND DISEASES.
ARTICLES IN THIS WEB SITE IS FOR YOUR REFERENCE ONLY. IF YOU HAVE ANY QUESTION, YOU SHOULD CONSULT WITH YOUR
DOCTOR IMMEDIATELY. ALL RIGHTS RESERVED 2008. DO NOT COPY NOR TRANSFER ARTICLES TO OTHER WEBSITES NOR OTHER
FORMS OF PUBLICATIONS. Privacy Policy. ARTICLE INDEX
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Denosumab is a fully human monoclonal antibody that specifically
targets a ligand known as RANKL (that binds to a receptor known as
RANK) which is a key mediator of osteoclast (the cells that break down
bone) formation, function, and survival. Denosumab is being studied
across a range of conditions including osteoporosis, treatment-induced
bone loss, bone metastases, multiple myeloma and rheumatoid arthritis.
RANK Ligand is found in all parts of cortical and trabecular bone.
In a Phase 3 study, twice-yearly subcutaneous injections of denosumab
increased bone mineral density (BMD) at all sites measured, including in
highly cortical areas of the skeleton. Cortical bone comprises 75 percent
of skeletal mass and is a primary determinant of overall strength in
vertebral and non-vertebral sites throughout the skeleton.
Denosumab treatment significantly increased lumbar spine BMD
compared with placebo at 24 months (6.5 percent vs. -0.6 percent; P
less than 0.0001). Denosumab also produced significant increases in
BMD at the total hip (3.4 percent vs. -1.1 percent), 1/3 distal radius
(wrist) (1.4 percent vs. -2.1 percent), and total body (2.4 percent vs. -1.4
percent). Time since menopause did not influence the BMD response to
denosumab. [1]
Data from a study of 2049 patients suffering from breast cancer that had
spread to the bone suggests that patients treated with denosumab were
free of skeletal injury -- including fracture, bone radiation or surgery, or
spinal cord compression -- for longer than patients treated with Novartis
AG's drug Zometa. [2]
Reference:
[1] Pivotal Phase 3 Data Show Denosumab Increased Bone Density at
Multiple Skeletal Sites in Early and Later Stage Postmenopausal Women
amgen.com Apr. 2, 2008.
[2] Amgen: Denosumab delays cancer-linked bone injury AP July 7, 2009
targets a ligand known as RANKL (that binds to a receptor known as
RANK) which is a key mediator of osteoclast (the cells that break down
bone) formation, function, and survival. Denosumab is being studied
across a range of conditions including osteoporosis, treatment-induced
bone loss, bone metastases, multiple myeloma and rheumatoid arthritis.
RANK Ligand is found in all parts of cortical and trabecular bone.
In a Phase 3 study, twice-yearly subcutaneous injections of denosumab
increased bone mineral density (BMD) at all sites measured, including in
highly cortical areas of the skeleton. Cortical bone comprises 75 percent
of skeletal mass and is a primary determinant of overall strength in
vertebral and non-vertebral sites throughout the skeleton.
Denosumab treatment significantly increased lumbar spine BMD
compared with placebo at 24 months (6.5 percent vs. -0.6 percent; P
less than 0.0001). Denosumab also produced significant increases in
BMD at the total hip (3.4 percent vs. -1.1 percent), 1/3 distal radius
(wrist) (1.4 percent vs. -2.1 percent), and total body (2.4 percent vs. -1.4
percent). Time since menopause did not influence the BMD response to
denosumab. [1]
Data from a study of 2049 patients suffering from breast cancer that had
spread to the bone suggests that patients treated with denosumab were
free of skeletal injury -- including fracture, bone radiation or surgery, or
spinal cord compression -- for longer than patients treated with Novartis
AG's drug Zometa. [2]
Reference:
[1] Pivotal Phase 3 Data Show Denosumab Increased Bone Density at
Multiple Skeletal Sites in Early and Later Stage Postmenopausal Women
amgen.com Apr. 2, 2008.
[2] Amgen: Denosumab delays cancer-linked bone injury AP July 7, 2009