Cathepsin K: Difference between revisions

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The protein encoded by this gene is a lysosomal [[cysteine protease]] involved in bone remodeling and resorption. This protein, which is a member of the peptidase C1 protein family, is expressed predominantly in [[osteoclast]]s.
The protein encoded by this gene is a lysosomal [[cysteine protease]] involved in bone remodeling and resorption. This protein, which is a member of the peptidase C1 protein family, is expressed predominantly in [[osteoclast]]s.


Cathepsin K is a [[protease]], which is defined by its high specificity for [[kinin]]s, that is involved in [[bone resorption]]. The enzyme's ability to catabolize [[elastin]], [[collagen]], and [[gelatin]] allow it to break down [[bone]] and [[cartilage]]. This catabolic activity is also partially responsible for the loss of lung elasticity and recoil in [[emphysema]]. Cathepsin K [[enzyme inhibitor|inhibitor]]s show great potential in the treatment of [[osteoporosis]]. Cathepsin K is degraded by Cathepsin S, called Controlled Cathepsin Cannibalism.
Cathepsin K is a [[protease]], which is defined by its high specificity for [[kinin]]s, that is involved in [[bone resorption]]. The enzyme's ability to catabolize [[elastin]], [[collagen]], and [[gelatin]] allows it to break down [[bone]] and [[cartilage]]. This catabolic activity is also partially responsible for the loss of lung elasticity and recoil in [[emphysema]]. Cathepsin K [[enzyme inhibitor|inhibitor]]s show great potential in the treatment of [[osteoporosis]]. Cathepsin K is degraded by Cathepsin S, called Controlled Cathepsin Cannibalism.


Cathepsin K expression is stimulated by [[inflammation|inflammatory]] [[cytokine]]s that are released after [[Biological tissue|tissue]] injury.
Cathepsin K expression is stimulated by [[inflammation|inflammatory]] [[cytokine]]s that are released after [[Biological tissue|tissue]] injury.
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Cathepsin K is expressed in a significant fraction of human [[breast cancer]]s, where it could contribute to tumor invasiveness.<ref name="Duong 2014">{{cite web | url=http://mct.aacrjournals.org/content/13/12/2898.long | title="Efficacy of a Cathepsin K Inhibitor in a Preclinical Model for Prevention and Treatment of Breast Cancer Bone Metastasis" | publisher=American Association for Cancer Research. | work=Molecular Cancer Therapeutics; 13(12); | date=23 September 2014 | accessdate=2 October 2016 | author=Duong, Le T.,  Wesolowski, Gregg A., Leung, Patrick  Oballa, Renata and Pickarski, Maureen | pages=2898–909}}</ref>  Mutations in this gene are the cause of [[pycnodysostosis]], an autosomal recessive disease characterized by [[osteosclerosis]] and short stature.<ref name="NCBI Gene Card cathepsin K">{{cite web | url=https://www.ncbi.nlm.nih.gov/gene?cmd=Retrieve&dopt=full_report&list_uids=1513 | title="CTSK cathepsin K [ Homo sapiens (human) ]" | publisher=National Center for Biotechnology Information, U.S. National Library of Medicine | work=NCBI Gene | date=4 September 2016 | accessdate=2 October 2016}}</ref> Cathepsin K has also been found to be over-expressed in [[glioblastoma]].<ref name="van Noorden 2014">{{cite web | url=http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0111819 | title="Expression Analysis of All Protease Genes Reveals Cathepsin K to Be Overexpressed in Glioblastoma" | publisher=LOCKSS | work=PLOS ONE | date=30 October 2014 | accessdate=2 October 2016 | author=Verbovšek, Urška, Motaln, Helena, Rotter, Ana, Atai, Nadia A., Gruden, Kristina, Van Noorden, Cornelis J.F., Lah, Tamara T.}}</ref>
Cathepsin K is expressed in a significant fraction of human [[breast cancer]]s, where it could contribute to tumor invasiveness.<ref name="Duong 2014">{{cite web | url=http://mct.aacrjournals.org/content/13/12/2898.long | title="Efficacy of a Cathepsin K Inhibitor in a Preclinical Model for Prevention and Treatment of Breast Cancer Bone Metastasis" | publisher=American Association for Cancer Research. | work=Molecular Cancer Therapeutics; 13(12); | date=23 September 2014 | accessdate=2 October 2016 | author=Duong, Le T.,  Wesolowski, Gregg A., Leung, Patrick  Oballa, Renata and Pickarski, Maureen | pages=2898–909}}</ref>  Mutations in this gene are the cause of [[pycnodysostosis]], an autosomal recessive disease characterized by [[osteosclerosis]] and short stature.<ref name="NCBI Gene Card cathepsin K">{{cite web | url=https://www.ncbi.nlm.nih.gov/gene?cmd=Retrieve&dopt=full_report&list_uids=1513 | title="CTSK cathepsin K [ Homo sapiens (human) ]" | publisher=National Center for Biotechnology Information, U.S. National Library of Medicine | work=NCBI Gene | date=4 September 2016 | accessdate=2 October 2016}}</ref> Cathepsin K has also been found to be over-expressed in [[glioblastoma]].<ref name="van Noorden 2014">{{cite web | url=http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0111819 | title="Expression Analysis of All Protease Genes Reveals Cathepsin K to Be Overexpressed in Glioblastoma" | publisher=LOCKSS | work=PLOS ONE | date=30 October 2014 | accessdate=2 October 2016 | author=Verbovšek, Urška, Motaln, Helena, Rotter, Ana, Atai, Nadia A., Gruden, Kristina, Van Noorden, Cornelis J.F., Lah, Tamara T.}}</ref>


That the expression of cathepsin K is characteristic for some cancers and not others has been documented.<ref name="Argani 2013">{{cite web | url=http://ajcp.oxfordjournals.org/content/139/2/151.long | title="A Broad Survey of Cathepsin K Immunoreactivity in Human Neoplasms" | publisher=Oxford Journals | work=American Journal of Clinical Pathology, Volume 139, Issue 2 | date=1 February 2013 | accessdate=2 October 2016 | author=Argani, Pedram, et al | pages=151–159}}</ref> Cathepsin K antibodies are marketed for research into expression of this enyzme by various cells.<ref name="NovusBiologicals">{{cite web | url=https://www.novusbio.com/primary-antibodies/cathepsin-k | title="Cathepsin K Antibodies" | publisher=Novus Biologicals, LLC | work=Novus Biologicals online catalog | date=2016 | accessdate=2 October 2016}}</ref><ref name="Abcam Catalog">{{cite web | url=http://www.abcam.com/cathepsin-k-antibody-ab19027.html | title="Anti-Cathepsin K antibody (ab19027)" | publisher=Abcam plc | work=Abcam plc online catalog | date=2016 | accessdate=2 October 2016}}</ref>
That the expression of cathepsin K is characteristic for some cancers and not others has been documented.<ref name="Argani 2013">{{cite web | url=http://ajcp.oxfordjournals.org/content/139/2/151.long | title="A Broad Survey of Cathepsin K Immunoreactivity in Human Neoplasms" | publisher=Oxford Journals | work=American Journal of Clinical Pathology, Volume 139, Issue 2 | date=1 February 2013 | accessdate=2 October 2016 | author=Argani, Pedram, et al | pages=151–159}}</ref> Cathepsin K antibodies are marketed for research into expression of this enyzme by various cells.<ref name="NovusBiologicals">{{cite web | url=https://www.novusbio.com/primary-antibodies/cathepsin-k | title="Cathepsin K Antibodies" | publisher=Novus Biologicals, LLC | work=Novus Biologicals online catalog | date=2016 | accessdate=2 October 2016}}</ref><ref name="Abcam Catalog">{{cite web | url=http://www.abcam.com/cathepsin-k-antibody-ab19027.html | title="Anti-Cathepsin K antibody (ab19027)" | publisher=Abcam plc | work=Abcam plc online catalog | date=2016 | accessdate=2 October 2016}}</ref><ref name="Antibodies.com">{{cite web | url=https://www.antibodies.com/cathepsin-k-antibody-a15026 | title="Anti-Cathepsin K Antibody (A5871)" | publisher=Antibodies.com Ltd|  work=Antibodies.com online catalog | date=2018 | accessdate=16 January 2018}}</ref>


[[Merck & Co.|Merck]] had a cathepsin K inhibitor, [[odanacatib]], in [[Phase III clinical trials]] for osteoporosis. In September, 2016, Merck announced they were discontinuing development of odanacatib after their own assessment of adverse events and an independent assessment showed increased risk of stroke.<ref name=" Bromme2009">{{cite web | url=http://www.tandfonline.com/doi/full/10.1517/13543780902832661%20 | title="Cathepsin K inhibitors for osteoporosis and potential off-target effects" | publisher=Taylor & Francis Online | work=Expert Opinion on Investigational Drugs, Volume 18 2009 - Issue 5 | date=24 April 2009 | accessdate=2 October 2016 | author=Brömme, Dieter, Lecaille, Fabien | pages=585–600}}</ref><ref name="MerckFinancial">{{cite web | url=http://investors.merck.com/investors/financial-news/press-release-details/2016/Merck-Provides-Update-on-Odanacatib-Development-Program/default.aspx | title="Merck Provides Update on Odanacatib Development Program" | publisher=Merck Sharp & Dohme Corp. | work= | date=2 September 2016 | accessdate=1 October 2016}}</ref>  Other cathepsin K inhbitors are in various stages of [[drug development|development]].<ref>Asagiri M, Hirai T, Kunigami T, Kamano S, Gober HJ, Okamoto K, Nishikawa K, Latz E, Golenbock DT, Aoki K, Ohya K, Imai Y, Morishita Y, Miyazono K, Kato S, Saftig P, Takayanagi H,. (2008). Cathepsin K-dependent toll-like receptor 9 signaling revealed in experimental arthritis. Science, 319(5863), 624-627.</ref><ref>Hussein, H., Ishihara, A., Menendez, M., & Bertone, A. (2014). Pharmacokinetics and bone resorption evaluation of a novel Cathepsin K inhibitor (VEL‐0230) in healthy adult horses. Journal of veterinary pharmacology and therapeutics.</ref><ref>{{Cite journal|last=Ren|first=Zhong-Yuan|last2=Machuca-Gayet|first2=Irma|last3=Domenget|first3=Chantal|last4=Buchet|first4=Rene|last5=Wu|first5=Yuqing|last6=Jurdic|first6=Pierre|last7=Mebarek|first7=Saida|date=2015-07-13|year=|title=Azanitrile Cathepsin K Inhibitors: Effects on Cell Toxicity, Osteoblast-Induced Mineralization and Osteoclast-Mediated Bone Resorption|journal=PLoS ONE|volume=10|issue=7|pages=|doi=10.1371/journal.pone.0132513|issn=1932-6203|pmc=4500499|pmid=26168340}}</ref>
[[Merck & Co.|Merck]] had a cathepsin K inhibitor, [[odanacatib]], in [[Phase III clinical trials]] for osteoporosis. In September, 2016, Merck announced they were discontinuing development of odanacatib after their own assessment of adverse events and an independent assessment showed increased risk of stroke.<ref name=" Bromme2009">{{cite web | url=http://www.tandfonline.com/doi/full/10.1517/13543780902832661%20 | title="Cathepsin K inhibitors for osteoporosis and potential off-target effects" | publisher=Taylor & Francis Online | work=Expert Opinion on Investigational Drugs, Volume 18 2009 - Issue 5 | date=24 April 2009 | accessdate=2 October 2016 | author=Brömme, Dieter, Lecaille, Fabien | pages=585–600}}</ref><ref name="MerckFinancial">{{cite web | url=http://investors.merck.com/investors/financial-news/press-release-details/2016/Merck-Provides-Update-on-Odanacatib-Development-Program/default.aspx | title="Merck Provides Update on Odanacatib Development Program" | publisher=Merck Sharp & Dohme Corp. | work= | date=2 September 2016 | accessdate=1 October 2016}}</ref>  Other cathepsin K inhibitors are in various stages of [[drug development|development]].<ref>Asagiri M, Hirai T, Kunigami T, Kamano S, Gober HJ, Okamoto K, Nishikawa K, Latz E, Golenbock DT, Aoki K, Ohya K, Imai Y, Morishita Y, Miyazono K, Kato S, Saftig P, Takayanagi H,. (2008). Cathepsin K-dependent toll-like receptor 9 signaling revealed in experimental arthritis. Science, 319(5863), 624-627.</ref><ref>Hussein, H., Ishihara, A., Menendez, M., & Bertone, A. (2014). Pharmacokinetics and bone resorption evaluation of a novel Cathepsin K inhibitor (VEL‐0230) in healthy adult horses. Journal of veterinary pharmacology and therapeutics.</ref><ref>{{Cite journal|last=Ren|first=Zhong-Yuan|last2=Machuca-Gayet|first2=Irma|last3=Domenget|first3=Chantal|last4=Buchet|first4=Rene|last5=Wu|first5=Yuqing|last6=Jurdic|first6=Pierre|last7=Mebarek|first7=Saida|date=2015-07-13|year=|title=Azanitrile Cathepsin K Inhibitors: Effects on Cell Toxicity, Osteoblast-Induced Mineralization and Osteoclast-Mediated Bone Resorption|journal=PLoS ONE|volume=10|issue=7|pages=|doi=10.1371/journal.pone.0132513|issn=1932-6203|pmc=4500499|pmid=26168340}}</ref> [[Medivir]] has a cathepsin K inhibitor, MIV-711 (L-006235<ref>{{Cite web|url=http://www.medivir.se/v5/en/RnD/proj_miv-711.cfm|title=MIV-711 for the treatment of ostheoarthritis|website=www.medivir.se|language=en|access-date=2017-10-06}}</ref><ref>{{Cite web|url=http://www.medivir.se/v5/images/pdf/2016/OARSI-poster-2016.pdf|title=THE CATHEPSIN K INHIBITOR L-006235 DEMONSTRATES BOTH DISEASE MODIFICATION AND ATTENUATION OF PAIN BEHAVIOUR IN THE IN THE MIA MODEL OF OSTEOARTHRITIS|last=James J. Burston,  Luting . Xu,  Paul I.  Mapp,  Urszula Grabowska, Karin Tunblad, Erik Lindström, Victoria Chapman|first=|date=April 2016|website=www.medivir.se|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite web|url=http://mb.cision.com/Main/652/2346448/722499.pdf|title=Data monitoring committee gives “Go Ahead” in the MIV-711 osteoarthritis extension study|last=|first=|date=14 September 2017|website=mb.cision.com|archive-url=|archive-date=|dead-url=|access-date=}}</ref>), in Phase IIa clinical trial, as a disease modifying osteoarthritis  drug, as of October 2017.
 
[[Medivir]] has a cathepsin K inhibitor, MIV-711 (aka. L-006235<ref>{{Cite web|url=http://www.medivir.se/v5/en/RnD/proj_miv-711.cfm|title=MIV-711 for the treatment of ostheoarthritis|website=www.medivir.se|language=en|access-date=2017-10-06}}</ref><ref>{{Cite web|url=http://www.medivir.se/v5/images/pdf/2016/OARSI-poster-2016.pdf|title=THE CATHEPSIN K INHIBITOR L-006235 DEMONSTRATES BOTH DISEASE MODIFICATION AND ATTENUATION OF PAIN BEHAVIOUR IN THE IN THE MIA MODEL OF OSTEOARTHRITIS|last=James J. Burston,  Luting . Xu,  Paul I.  Mapp,  Urszula Grabowska, Karin Tunblad, Erik Lindström, Victoria Chapman|first=|date=April 2016|website=www.medivir.se|archive-url=|archive-date=|dead-url=|access-date=}}</ref><ref>{{Cite web|url=http://mb.cision.com/Main/652/2346448/722499.pdf|title=Data monitoring committee gives “Go Ahead” in the MIV-711 osteoarthritis extension study|last=|first=|date=14 September 2017|website=mb.cision.com|archive-url=|archive-date=|dead-url=|access-date=}}</ref>), in Phase IIa clinical trial, as a DMOAD (Disease Modifying [[Osteoarthritis]] Drug), as of October 2017.


==References==
==References==
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*{{cite journal  | vauthors=Brömme D, Okamoto K |title=Human cathepsin O2, a novel cysteine protease highly expressed in osteoclastomas and ovary molecular cloning, sequencing and tissue distribution. |journal=Biol. Chem. Hoppe-Seyler |volume=376 |issue= 6 |pages= 379–84 |year= 1995 |pmid= 7576232 |doi=  10.1515/bchm3.1995.376.6.379}}
*{{cite journal  | vauthors=Brömme D, Okamoto K |title=Human cathepsin O2, a novel cysteine protease highly expressed in osteoclastomas and ovary molecular cloning, sequencing and tissue distribution. |journal=Biol. Chem. Hoppe-Seyler |volume=376 |issue= 6 |pages= 379–84 |year= 1995 |pmid= 7576232 |doi=  10.1515/bchm3.1995.376.6.379}}
*{{cite journal  | vauthors=Gelb BD, Edelson JG, Desnick RJ |title=Linkage of pycnodysostosis to chromosome 1q21 by homozygosity mapping. |journal=Nat. Genet. |volume=10 |issue= 2 |pages= 235–7 |year= 1995 |pmid= 7663521 |doi= 10.1038/ng0695-235 }}
*{{cite journal  | vauthors=Gelb BD, Edelson JG, Desnick RJ |title=Linkage of pycnodysostosis to chromosome 1q21 by homozygosity mapping. |journal=Nat. Genet. |volume=10 |issue= 2 |pages= 235–7 |year= 1995 |pmid= 7663521 |doi= 10.1038/ng0695-235 }}
*{{cite journal  | vauthors=Polymeropoulos MH, Ortiz De Luna RI, Ide SE |title=The gene for pycnodysostosis maps to human chromosome 1cen-q21. |journal=Nat. Genet. |volume=10 |issue= 2 |pages= 238–9 |year= 1995 |pmid= 7663522 |doi= 10.1038/ng0695-238 |display-authors=etal}}
*{{cite journal  | vauthors=Polymeropoulos MH, Ortiz De Luna RI, Ide SE |title=The gene for pycnodysostosis maps to human chromosome 1cen-q21. |journal=Nat. Genet. |volume=10 |issue= 2 |pages= 238–9 |year= 1995 |pmid= 7663522 |doi= 10.1038/ng0695-238 |display-authors=etal|url=https://zenodo.org/record/1233385/files/article.pdf }}
*{{cite journal  | vauthors=Shi GP, Chapman HA, Bhairi SM |title=Molecular cloning of human cathepsin O, a novel endoproteinase and homologue of rabbit OC2. |journal=FEBS Lett. |volume=357 |issue= 2 |pages= 129–34 |year= 1995 |pmid= 7805878 |doi=10.1016/0014-5793(94)01349-6  |display-authors=etal}}
*{{cite journal  | vauthors=Shi GP, Chapman HA, Bhairi SM |title=Molecular cloning of human cathepsin O, a novel endoproteinase and homologue of rabbit OC2. |journal=FEBS Lett. |volume=357 |issue= 2 |pages= 129–34 |year= 1995 |pmid= 7805878 |doi=10.1016/0014-5793(94)01349-6  |display-authors=etal}}
*{{cite journal  | vauthors=Inaoka T, Bilbe G, Ishibashi O |title=Molecular cloning of human cDNA for cathepsin K: novel cysteine proteinase predominantly expressed in bone. |journal=Biochem. Biophys. Res. Commun. |volume=206 |issue= 1 |pages= 89–96 |year= 1995 |pmid= 7818555 |doi= 10.1006/bbrc.1995.1013 |display-authors=etal}}
*{{cite journal  | vauthors=Inaoka T, Bilbe G, Ishibashi O |title=Molecular cloning of human cDNA for cathepsin K: novel cysteine proteinase predominantly expressed in bone. |journal=Biochem. Biophys. Res. Commun. |volume=206 |issue= 1 |pages= 89–96 |year= 1995 |pmid= 7818555 |doi= 10.1006/bbrc.1995.1013 |display-authors=etal}}

Latest revision as of 03:36, 8 December 2018

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Identifiers
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External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

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RefSeq (mRNA)

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RefSeq (protein)

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Wikidata
View/Edit Human

Cathepsin K, abbreviated CTSK, is an enzyme that in humans is encoded by the CTSK gene.[1][2]

Function

The protein encoded by this gene is a lysosomal cysteine protease involved in bone remodeling and resorption. This protein, which is a member of the peptidase C1 protein family, is expressed predominantly in osteoclasts.

Cathepsin K is a protease, which is defined by its high specificity for kinins, that is involved in bone resorption. The enzyme's ability to catabolize elastin, collagen, and gelatin allows it to break down bone and cartilage. This catabolic activity is also partially responsible for the loss of lung elasticity and recoil in emphysema. Cathepsin K inhibitors show great potential in the treatment of osteoporosis. Cathepsin K is degraded by Cathepsin S, called Controlled Cathepsin Cannibalism.

Cathepsin K expression is stimulated by inflammatory cytokines that are released after tissue injury.

Clinical significance

Cathepsin K is expressed in a significant fraction of human breast cancers, where it could contribute to tumor invasiveness.[3] Mutations in this gene are the cause of pycnodysostosis, an autosomal recessive disease characterized by osteosclerosis and short stature.[4] Cathepsin K has also been found to be over-expressed in glioblastoma.[5]

That the expression of cathepsin K is characteristic for some cancers and not others has been documented.[6] Cathepsin K antibodies are marketed for research into expression of this enyzme by various cells.[7][8][9]

Merck had a cathepsin K inhibitor, odanacatib, in Phase III clinical trials for osteoporosis. In September, 2016, Merck announced they were discontinuing development of odanacatib after their own assessment of adverse events and an independent assessment showed increased risk of stroke.[10][11] Other cathepsin K inhibitors are in various stages of development.[12][13][14] Medivir has a cathepsin K inhibitor, MIV-711 (L-006235[15][16][17]), in Phase IIa clinical trial, as a disease modifying osteoarthritis drug, as of October 2017.

References

  1. ↑ "Entrez Gene: CTSK cathepsin K".
  2. ↑ Inaoka T, Bilbe G, Ishibashi O, Tezuka K, Kumegawa M, Kokubo T (January 1995). "Molecular cloning of human cDNA for cathepsin K: novel cysteine proteinase predominantly expressed in bone". Biochem. Biophys. Res. Commun. 206 (1): 89–96. doi:10.1006/bbrc.1995.1013. PMID 7818555.
  3. ↑ Duong, Le T., Wesolowski, Gregg A., Leung, Patrick Oballa, Renata and Pickarski, Maureen (23 September 2014). ""Efficacy of a Cathepsin K Inhibitor in a Preclinical Model for Prevention and Treatment of Breast Cancer Bone Metastasis"". Molecular Cancer Therapeutics; 13(12);. American Association for Cancer Research. pp. 2898–909. Retrieved 2 October 2016.
  4. ↑ ""CTSK cathepsin K [ Homo sapiens (human) ]"". NCBI Gene. National Center for Biotechnology Information, U.S. National Library of Medicine. 4 September 2016. Retrieved 2 October 2016.
  5. ↑ Verbovšek, Urška, Motaln, Helena, Rotter, Ana, Atai, Nadia A., Gruden, Kristina, Van Noorden, Cornelis J.F., Lah, Tamara T. (30 October 2014). ""Expression Analysis of All Protease Genes Reveals Cathepsin K to Be Overexpressed in Glioblastoma"". PLOS ONE. LOCKSS. Retrieved 2 October 2016.
  6. ↑ Argani, Pedram; et al. (1 February 2013). ""A Broad Survey of Cathepsin K Immunoreactivity in Human Neoplasms"". American Journal of Clinical Pathology, Volume 139, Issue 2. Oxford Journals. pp. 151–159. Retrieved 2 October 2016.
  7. ↑ ""Cathepsin K Antibodies"". Novus Biologicals online catalog. Novus Biologicals, LLC. 2016. Retrieved 2 October 2016.
  8. ↑ ""Anti-Cathepsin K antibody (ab19027)"". Abcam plc online catalog. Abcam plc. 2016. Retrieved 2 October 2016.
  9. ↑ ""Anti-Cathepsin K Antibody (A5871)"". Antibodies.com online catalog. Antibodies.com Ltd. 2018. Retrieved 16 January 2018.
  10. ↑ Brömme, Dieter, Lecaille, Fabien (24 April 2009). ""Cathepsin K inhibitors for osteoporosis and potential off-target effects"". Expert Opinion on Investigational Drugs, Volume 18 2009 - Issue 5. Taylor & Francis Online. pp. 585–600. Retrieved 2 October 2016.
  11. ↑ ""Merck Provides Update on Odanacatib Development Program"". Merck Sharp & Dohme Corp. 2 September 2016. Retrieved 1 October 2016.
  12. ↑ Asagiri M, Hirai T, Kunigami T, Kamano S, Gober HJ, Okamoto K, Nishikawa K, Latz E, Golenbock DT, Aoki K, Ohya K, Imai Y, Morishita Y, Miyazono K, Kato S, Saftig P, Takayanagi H,. (2008). Cathepsin K-dependent toll-like receptor 9 signaling revealed in experimental arthritis. Science, 319(5863), 624-627.
  13. ↑ Hussein, H., Ishihara, A., Menendez, M., & Bertone, A. (2014). Pharmacokinetics and bone resorption evaluation of a novel Cathepsin K inhibitor (VEL‐0230) in healthy adult horses. Journal of veterinary pharmacology and therapeutics.
  14. ↑ Ren, Zhong-Yuan; Machuca-Gayet, Irma; Domenget, Chantal; Buchet, Rene; Wu, Yuqing; Jurdic, Pierre; Mebarek, Saida (2015-07-13). "Azanitrile Cathepsin K Inhibitors: Effects on Cell Toxicity, Osteoblast-Induced Mineralization and Osteoclast-Mediated Bone Resorption". PLoS ONE. 10 (7). doi:10.1371/journal.pone.0132513. ISSN 1932-6203. PMC 4500499. PMID 26168340.
  15. ↑ "MIV-711 for the treatment of ostheoarthritis". www.medivir.se. Retrieved 2017-10-06.
  16. ↑ James J. Burston, Luting . Xu, Paul I. Mapp, Urszula Grabowska, Karin Tunblad, Erik Lindström, Victoria Chapman (April 2016). "THE CATHEPSIN K INHIBITOR L-006235 DEMONSTRATES BOTH DISEASE MODIFICATION AND ATTENUATION OF PAIN BEHAVIOUR IN THE IN THE MIA MODEL OF OSTEOARTHRITIS" (PDF). www.medivir.se.
  17. ↑ "Data monitoring committee gives "Go Ahead" in the MIV-711 osteoarthritis extension study" (PDF). mb.cision.com. 14 September 2017.

Further reading

Additional images

External links


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