Supplemented and unsupplemented tissue sealants, methods of...

Drug – bio-affecting and body treating compositions – Preparations characterized by special physical form – Implant or insert

Reexamination Certificate

Rate now

  [ 0.00 ] – not rated yet Voters 0   Comments 0

Details

C424S078060, C424S078070, C424S400000, C424S422000, C424S423000, C424S425000, C424S426000, C424S488000, C424S499000, C530S380000, C530S381000, C530S382000, C623S016110, C623S018110, C623S019140, C623S020230, C623S021180, C623S022290, C623S023480

Reexamination Certificate

active

06197325

ABSTRACT:

FIELD OF INVENTION
This invention is directed to unsupplemented and supplemented Tissue Sealants (TS), such as fibrin glue (FG), as well as to methods of their production and use. In one embodiment, this invention is directed to TSs which do not inhibit full-thickness skin wound healing. In another embodiment, this invention is directed to TSs which have been supplemented with a growth factor(s) and/or a drug(s), as well as to methods of their production and use. The particular growth factor(s) or drug(s) that is selected is a function of its use.
BACKGROUND OF THE INVENTION
A. Wound Healing and Growth Factors
Wound healing, the repair of lesions, begins almost instantly after injury. It requires the successive coordinated function of a variety of cells and the close regulation of degradative and regenerative steps. The proliferation, differentiation and migration of cells are important biological processes which underlie wound healing, which also involves fibrin clot formation, resorption of the clot, tissue remodeling, such as fibrosis, endothelialization and epithelialization. Wound healing involves the formation of highly vascularized tissue that contains numerous capillaries, many active fibroblasts, and abundant collagen fibrils, but not the formation of specialized skin structures.
The process of wound healing can be initiated by thromboplastin which flows out of injured cells. Thromboplastin contacts plasma factor VII to form factor X activator, which then, with factor V and in a complex with phospholipids and calcium, converts prothrombin into thrombin. Thrombin catalyzes the release of fibrinopeptides A and B from fibrinogen to produce fibrin monomers, which aggregate to form fibrin filaments. Thrombin also activates the transglutaminase, factor XIIIa, which catalyzes the formation of isopeptide bonds to covalently cross-link the fibrin filaments. Alpha
2
-antiplasmin is then bound by factor XIII onto the fibrin filaments to thereby protect the filaments from degradation by plasmin (see, for example, Doolittle et al.,
Ann. Rev. Biochem.
53:195-229 (1984)).
When a tissue is injured, polypeptide growth factors, which exhibit an array of biological activities, are released into the wound where they play a crucial role in healing (see, e.g.,
Hormonal Proteins and Peptides
(Li, C. H., ed.) Volume 7, Academic Press, Inc., New York, N.Y. pp. 231-277 (1979) and Brunt et al.,
Biotechnology
6:25-30 (1988)). These activities include recruiting cells, such as leukocytes and fibroblasts, into the injured area, and inducing cell proliferation and differentiation. Growth factors that may participate in wound healing include, but are not limited to: platelet-derived growth factors (PDGFs); insulin-binding growth factor-1 (IGF-1); insulin-binding growth factor-2 (IGF-2); epidermal growth factor (EGF); transforming growth factor-&agr; (TGF-&agr;); transforming growth factor-&bgr; (TGF-&bgr;); platelet factor 4 (PF4); and heparin binding growth factors one and two (HBGF-1 and HBGF-2, respectively).
PDGFs are stored in the alpha granules of circulating platelets and are released at wound sites during blood clotting (see, e.g., Lynch et al.,
J. Clin. Invest.
84:640-646 (1989)). PDGFs include: PDGF; platelet derived angiogenesis factor (PDAF); TGF-&bgr;; and PF4, which is a chemoattractant for neutrophils (Knighton et al., in
Growth Factors and Other Aspects of Wound Healing: Biological and Clinical Implications,
Alan R. Liss, Inc., New York, N.Y., pp. 319-329 (1988)). PDGF is a mitogen, chemoattractant and a stimulator of protein synthesis in cells of mesenchymal origin, including fibroblasts and smooth muscle cells. PDGF is also a nonmitogenic chemoattractant for endothelial cells (see, for example, Adelmann-Grill et al.,
Eur. J. Cell Biol.
51:322-326 (1990)).
IGF-1 acts in combination with PDGF to promote mitogenesis and protein synthesis in mesenchymal cells in culture. Application of either PDGF or IGF-1 alone to skin wounds does not enhance healing, but application of both factors together appears to promote connective tissue and epithelial tissue growth (Lynch et al.,
Proc. Natl. Acad. Sci.
76:1279-1283 (1987)) .
TGF-&bgr; is a chemoattractant for macrophages and monocytes. Depending upon the presence or absence of other growth factors, TGF-&bgr; may stimulate or inhibit the growth of many cell types. For example, when applied in vivo, TGF-&bgr; increases the tensile strength of healing dermal wounds. TGF-&bgr; also inhibits endothelial cell mitosis, and stimulates collagen and glycosaminoglycan synthesis by fibroblasts.
Other growth factors, such as EGF, TGF-&agr;, the HBGFs and osteogenin are also important in wound healing. EGF, which is found in gastric secretions and saliva, and TGF-&agr;, which is made by both normal and transformed cells, are structurally related and may recognize the same receptors. These receptors mediate proliferation of epithelial cells. Both factors accelerate reepithelialization of skin wounds. Exogenous EGF promotes wound healing by stimulating the proliferation of keratinocytes and dermal fibroblasts (Nanney et al.,
J. Invest. Dermatol.
83:385-393 (1984) and Coffey et al.,
Nature
328:817-820 (1987)). Topical application of EGF accelerates the rate of healing of partial thickness wounds in humans (Schultz et al.,
Science
235:350-352 (1987)). Osteogenin, which has been purified from demineralized bone, appears to promote bone growth (see, e.g., Luyten et al.,
J. Biol. Chem.
264:13377 (1989)). In addition, platelet-derived wound healing formula, a platelet extract which is in the form of a salve or ointment for topical application, has been described (see, e.g., Knighton et al.,
Ann. Surg.
204:322-330 (1986)).
The Heparin Binding Growth Factors (HBGFs), also known as Fibroblast Growth Factors (FGFs), which include acidic HBGF (aHBGF also known as HBFG-1 or FGF-1) and basic HBGF (bHBGF also known as HBGF-2 or FGF-2), are potent mitogens for cells of mesodermal and neuroectodermal lineages, including endothelial cells (see, e.g., Burgess et al.,
Ann. Rev. Biochem.
58:575-606 (1989)). In addition, HBGF-1 is chemotactic for endothelial cells and astroglial cells. Both HBGF-l and HBGF-2 bind to heparin, which protects them from proteolytic degradation. The array of biological activities exhibited by the HBGFs suggests that they play an important role in wound healing.
Basic fibroblast growth factor (FGF-2) is a potent stimulator of angiogenesis and the migration and proliferation of fibroblasts (see, for example, Gospodarowicz et al.,
Mol. Cell. Endocinol.
46:187-204 (1986) and Gospodarowicz et al.,
Endo. Rev.
8:95-114 (1985)). Acidic fibroblast growth factor (FGF-1) has been shown to be a potent angiogenic factor for endothelial cells (Burgess et al., supra, 1989). However, it has not been established if any FGF growth factor is chemotactic for fibroblasts.
Growth factors are, therefore, potentially useful for specifically promoting wound healing and tissue repair. However, their use to promote wound healing has yielded inconsistent results (see, e.g., Carter et al., in
Growth Factors and Other Aspects of Wound Healing: Biological and Clinical Implications,
Alan R. Liss, Inc., New York, New York, pp. 303-317 (1988)). For example, PDGF, IGF-1, EGF, TGF-&agr;, TGF-&bgr; and FGF (also known as HBGF) applied separately to standardized skin wounds in swine had little effect on the regeneration of connective tissue or epithelium in the wounds (Lynch et al.,
J. Clin. Invest.
84:640-646 (1989)). Of the factors tested, TGF-&bgr; stimulated the greatest response alone. However, a combination of factors, such as PDGF-bb homodimer and IGF-1 or TGF-&agr; produced a dramatic increase in connective tissue regeneration and epithelialization. (Id.) Tsuboi et al. have reported that the daily application of bFGF to an open wound stimulated wound healing in healing-impaired mice but not in normal mice (
J. Exp. Med.
172:245-251 (1990)). On the other hand, the application to human skin wounds of crude preparations of porcine or bovine platele

LandOfFree

Say what you really think

Search LandOfFree.com for the USA inventors and patents. Rate them and share your experience with other people.

Rating

Supplemented and unsupplemented tissue sealants, methods of... does not yet have a rating. At this time, there are no reviews or comments for this patent.

If you have personal experience with Supplemented and unsupplemented tissue sealants, methods of..., we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Supplemented and unsupplemented tissue sealants, methods of... will most certainly appreciate the feedback.

Rate now

     

Profile ID: LFUS-PAI-O-2445325

  Search
All data on this website is collected from public sources. Our data reflects the most accurate information available at the time of publication.