Wint™ is a unique, high-performance separation device designed to obtain blood derived product rich in DKK-1 (Dickkopf-1) protein- a natural, endogenous inhibitor of Wnt signaling pathway from patient’s own blood. Wint™ separation device, due to presence of the exclusive borosilicate activator triggers the release of DKK-1 protein from the isolated and concentrated platelets (PLTs).

Due to is unique properties and carefully designated activator, Wint™ separation device enables to acquire nearly 6x increased concentration of the DKK-1 protein in the autologous blood derived product, simultaneously with the absence of the pro-inflammatory factors1.
Since Wint™ separation device allows to obtain a final product dedicated for intra-articular injection abundant in DKK-1 protein, subsequent therapy based on this blood derived product aims to inhibit the deleterious Wnt signaling pathway in the joint tissues.

Finally, by blocking the Wnt signaling pathway with endogenous, platelet-derived DKK-1 protein the therapy aims to stop the progression of the disease in OA affected joint2,3.
  1. Data on file Biovico
  2. Wang, Y., Fan, X., Xing, L., & Tian, F. (2019). Wnt signaling: a promising target for osteoarthritis therapy. Cell Communication and Signaling, 17(1), 1-14.
  3. Honsawek, S., Tanavalee, A., Yuktanandana, P., Ngarmukos, S., Saetan, N., & Tantavisut, S. (2010). Dickkopf-1 (Dkk-1) in plasma and synovial fluid is inversely correlated with radiographic severity of knee osteoarthritis patients. BMC musculoskeletal disorders, 11, 1-7.
Currently there is no therapy that can completely stop the progression of OA. There is also no possibility to reverse the effects of already existing changes, so the currently available therapies are dedicated only to reduce the symptoms of the disease.

Because of that, recently a search for a solution, based on targeted therapies that act on the molecular signaling levels become more effective. Unfortunately, previous experience showed that therapy based on interleukin 1 receptor antagonist (IL-1Ra) did not fulfill its first expectations1. The researchers’ attention has now focused on the Wnt signaling pathway as a one of the major factors responsible for the OA progression2. Increased activation of the Wnt signaling pathway plays a major role in the development and progression of OA, by controlling the function of synovial cells, chondrocytes and osteoblasts, so affecting3,4:
{|blog_list|}
  • Bone remodeling
  • Osteoblast apoptosis
  • Synovium inflammation
  • Articular cartilage metabolism
  • Extracellular matrix catabolism

Because of that, the global direction of OA therapy focuses on blocking the overactive canonical Wnt signaling pathway in the synovial joint tissues at the molecular level. Attention has been now focused on natural inhibitors of the Wnt signaling pathway, of which DKK-1 plays an important role5.

Scientific and clinical data show that therapy based on Wnt signaling pathway inhibition can be a respectful treatment for joint environment deterioration6. DKK-1 protein, acting as a inhibitor, influence the signaling pathway of Wnt by deactivating it. High abundance of DKK-1 protein protects articular cartilage from degradation and finally slows the progression of the osteoarthritis7.

Motivated by this Wint™ kit procedure pack contains a highly efficient separation device, which due to its unique design and presence of carefully selected borosilicate PLT activator allows to separate and isolate a very high number of DKK-1 protein in the final injection product.

As a result, the blood-derived product acquired by Wint™ separation device allows to obtain approximately 3x higher DKK-1 protein concentration than in platelet-rich plasma product and 6x higher DKK-1 protein concentration than can be detected in the plasma of healthy patient’s6.

Wint™ kit provides 1 mL of autologous blood-derived product featured with increased concentration of DKK-1 protein from 13.5 mL of patient’s peripheral blood dedicated for the targeted therapy in OA affected joint.
Taking into consideration the product autologous characteristics, so: lack of possibility for triggering of the patients uncontrolled immune response7 and no possibility for donor-recipient disease transmission, the therapy based on the product obtained with the Wint™ kit is considered as fully safe for intra-articular administration.


Package of Wint™ kit contains:

  • Wint™ separation device (1 pc)
  • Venofix® A, 21G butterfly needle (1 pc)
  • Microlance™ 3, 21Gx1½” needle (2 pcs)
  • Microlance™ 3, 27Gx¾” needle (1 pc)
  • Microlance™ 3, 19Gx1½” needle (1 pc)
  • dicoNEX Single use syringe, 20 mL (1 pc)
  • dicoNEX Single use syringe, 10 mL (1 pc)
  • dicoNEX Single use syringe, 2 mL (1 pc)
Recent clinical data shows that Wint™ administration is clinically effective in OA patients when administered as a single intra-articular injection, what brings up to 6 months in OA symptoms improvement10.

The product is meant to use by medical practitioners only.

  1. Chevalier X, Eymard F. Anti-IL-1 for the treatment of OA: dead or alive? Nat Rev Rheumatol. 2019 Apr;15(4):191-192.
  2. Wang Y, Fan X, Xing L, Tian F. Wnt signaling: a promising target for osteoarthritis therapy. Cell Commun Signal. 2019 Aug 16;17(1):97.
  3. Koziński K, Dobrzyń A. Szlak sygnałowy Wnt i jego rola w regulacji metabolizmu komórki [Wnt signaling pathway--its role in regulation of cell metabolism]. Postepy Hig Med Dosw (Online). 2013 Nov 26;67:1098-108. Polish
  4. Lories RJ, Monteagudo S. Review Article: Is Wnt Signaling an Attractive Target for the Treatment of Osteoarthritis? Rheumatol Ther. 2020 Jun;7(2):259-270.
  5. Ueland T, Otterdal K, Lekva T, Halvorsen B, Gabrielsen A, Sandberg WJ, Paulsson-Berne G, Pedersen TM, Folkersen L, Gullestad L, Oie E, Hansson GK, Aukrust P. Dickkopf-1 enhances inflammatory interaction between platelets and endothelial cells and shows increased expression in atherosclerosis. Arterioscler Thromb Vasc Biol. 2009 Aug;29(8):1228-34.
  6. Deshmukh V, O'Green AL, Bossard C, Seo T, Lamangan L, Ibanez M, Ghias A, Lai C, Do L, Cho S, Cahiwat J, Chiu K, Pedraza M, Anderson S, Harris R, Dellamary L, Kc S, Barroga C, Melchior B, Tam B, Kennedy S, Tambiah J, Hood J, Yazici Y. Modulation of the Wnt pathway through inhibition of CLK2 and DYRK1A by lorecivivint as a novel, potentially disease-modifying approach for knee osteoarthritis treatment. Osteoarthritis Cartilage. 2019 Sep;27(9):1347-1360.
  7. Honsawek, S., Tanavalee, A., Yuktanandana, P., Ngarmukos, S., Saetan, N., & Tantavisut, S. (2010). Dickkopf-1 (Dkk-1) in plasma and synovial fluid is inversely correlated with radiographic severity of knee osteoarthritis patients. BMC musculoskeletal disorders, 11, 1-7.
  8. Data on Biovico I.
  9. Yogev, Y. (2020). A humoral solution: Autologous blood products and tissue repair. Cellular Immunology, 356, 104178.
  10. Data on Biovico II. 
Hyaluronic acid and viscosupplementation
Wnt signaling pathway plays a pivotal role in a various processes. The development of the articular joints, including cartilage tissue and joint cavity is one of them1. Taking this into consideration the occurrence and progression of the degenerative joint diseases, such as osteoarthritis (OA) is described to be linked with Wnt pathway2. Wnt pathway is activated when the Wnt protein ligand binds itself to a specific receptors located on the cell membrane of e.g. chondrocytes or synovial like fibroblasts. That action leads to destabilization of the β-catenin degradation complex and what follows, the cumulation of this protein in the cytoplasm. Subsequently, accumulated β-catenin molecules are able to migrate to the cell nuclei (acting as a transcription factors) and by this they influence transcription of wide range of genes, including ones that are responsible for the progression of the OA3.
{|blog_list|}
Therapeutic rationale of DKK-1 protein-enriched blood derived product in OA affected joints 
Current strategy in OA therapies focuses on blocking the overactive canonical Wnt signaling pathway in the synovial joint tissues at the molecular level. There are numbers of known chemical inhibitors, but DKK-1 is one of the most potent and, what is important, it is endogenously produced Wnt signaling pathway inhibitor.

When DKK-1 protein binds to the Wnt signaling pathway receptor it blocks the specific binding site of the Wnt ligand protein, preventing further pathway activation. This leads to β-catenin degradation complex activation and further β-catenin molecules degradation. Lack of β-catenin proteins in cell cytoplasm prevents the transcription mechanism activation and the factors responsible for OA progression cannot be produced by the chondrocytes or synovial like fibroblasts4.

Interestingly, PLTs are known, rich source of DKK-1 protein. When properly activated and stimulated, platelets can secrete increased amounts of this natural inhibitor. Thus, activated autologous blood-derived products, after the separation and concentration can provide an abundance of Wnt signaling pathway inhibitor. Further intra-articular administration of this can lead to the reduction of the degradation of articular cartilage and diminishing of the joint inflammation5.

Intra-articular Injection of the product obtained by the Wint™ kit is a highly recommendable therapy for joint associated pathologies. Based on the literature and experience, the therapy which uses autologous blood-derived product enriched with DKK-1 protein was estimated as an therapeutically effective against OA symptoms6.
Supporting evidences for the validity of Wnt signaling pathway inhibition by DKK-1 in OA: 
  • In OA patients a decreased levels of DKK-1 in plasma and synovial fluid are observed7
  • It has been shown that the level of DKK-1 protein highly is related to the stage of the osteoarthritis → the higher stage of the disease, the lower concentration of DKK-1 in the patient’s plasma7
  • Increased production of DKK-1 in synovial cells, chondrocytes and osteoblasts protects the articular cartilage from degradation and diminishes the progression of OA7,4
  1. Yamagami T, Molotkov A, Zhou CJ. Canonical Wnt signaling activity during synovial joint development. J Mol Hist. 2009;40(4):311-316. doi:10.1007/s10735-009-9242-1
  2. Van Den Bosch MH, Blom AB, Sloetjes AW, et al. Induction of Canonical Wnt Signaling by Synovial Overexpression of Selected Wnts Leads to Protease Activity and Early Osteoarthritis-Like Cartilage Damage. The American Journal of Pathology. 2015;185(7):1970-1980. doi:10.1016/j.ajpath.2015.03.013
  3. Corr M. Wnt–β-catenin signaling in the pathogenesis of osteoarthritis. Nat Rev Rheumatol. 2008;4(10):550-556. doi:10.1038/ncprheum0904
  4. Wang Y, Fan X, Xing L, Tian F. Wnt signaling: a promising target for osteoarthritis therapy. Cell Commun Signal. 2019;17(1):97. doi:10.1186/s12964-019-0411-x
  5. Ueland T, Otterdal K, Lekva T, et al. Dickkopf-1 Enhances Inflammatory Interaction Between Platelets and Endothelial Cells and Shows Increased Expression in Atherosclerosis. ATVB. 2009;29(8):1228-1234. doi:10.1161/ATVBAHA.109.189761
  6. Pérez‐García S, Carrión M, Villanueva‐Romero R, et al. Wnt and RUNX2 mediate cartilage breakdown by osteoarthritis synovial fibroblast‐derived ADAMTS‐7 and ‐12. J Cell Mol Med. 2019;23(6):3974-3983. doi:10.1111/jcmm.14283
  7. Honsawek S, Tanavalee A, Yuktanandana P, Ngarmukos S, Saetan N, Tantavisut S. Dickkopf-1 (Dkk-1) in plasma and synovial fluid is inversely correlated with radiographic severity of knee osteoarthritis patients. BMC Musculoskelet Disord. 2010 Nov 10;11:257.

No materials available.