SVVYGLR 

SVVYGLR is an osteopontin-derived peptide. SVVYGLR can promote the differentiation of fibroblasts into myofibroblast-like cells and promote the production of type III collagen by cardiac fibroblasts. SVVYGLR can activate the adhesion, migration and tubule formation of endothelial cells in vitro. SVVYGLR promotes angiogenesis and wound healing and promotes the migration of dermal fibroblasts and keratinocytes. SVVYGLR can be used for research related to angiogenesis, dermal wounds and bone regeneration^[1][2][3].

SVVYGLR (0.02 μg/mL) activates adhesion, migration, and tube formation by endothelial cells in vitro^[1].
SVVYGLR (0.01-100 μg/mL; 2 h coating, 30 min cell incubation) enhances adhesion of hMSCs, hPLFs, hGFs, and HUVECs in a concentration-dependent manner, with the strongest effect at 100 μg/mL^[2].
SVVYGLR (1-1000 ng/mL; continuous culture with medium renewal every other day, measured on day 6) enhances proliferation of hMSCs, HUVECs, and hPLFs (but not hGFs) in a concentration-dependent manner, with the strongest effect at 100 ng/mL on day 6^[2].
SVVYGLR (10-1000 ng/mL; 5 days for RAW264.7 cells, 10 days for BMMs) suppresses osteoclastogenesis in RAW264.7 cells and BMMs, with significant inhibition at 100 ng/mL^[2].
SVVYGLR (100 ng/mL; 24, 72, 96 h) suppresses RANKL-induced NFAT activity in pNFAT/Luc-RAW264.7 cells at 100 ng/mL^[2].
SVVYGLR (100 ng/mL; 3, 5 days) downregulates expression of osteoclastogenic marker genes (calcitonin receptor, cathepsin K, TRAP) and integrin α9 in RANKL-stimulated RAW264.7 cells at 100 ng/mL^[2].
SVVYGLR (10 ng/mL; 36 h) significantly accelerates the migration of rat dermal fibroblasts (RDFs) into scratch wound areas at 36 h^[3].
SVVYGLR (10 ng/mL; 10 h) significantly accelerates the migration of human epithelial keratinocytes (HEKa) into scratch wound areas at 10 h^[3].
SVVYGLR (10 ng/mL; 3 h) significantly enhances the migratory activity of rat dermal fibroblasts (RDFs) and human epithelial keratinocytes (HEKa) in a 3-hour Chemotaxicell migration assay^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

SVVYGLR (0.02 µg/mL; implanted via diffusion chamber; 5 days) induces significant in vivo angiogenesis in the dorsal air sac mouse model, with a mean angiogenesis grade of 2.00^[1].
SVVYGLR (10 µg; implanted via collagen sponge; single administration at the time of defect creation) suppresses osteoclast numbers in bone defects at 3 weeks and enhances collagen sponge resorption and compact bone formation by 5 weeks in a rat calvarial defect model^[2].
SVVYGLR (12.5 μg/gel; topical via Medgel; single application at wound creation) promotes dermal wound healing by stimulating fibroblast migration, myofibroblastic differentiation of fibroblasts, and angiogenesis in rats^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

792.92

C₃₆H₆₀N₁₀O₁₀

292851-89-9

Ser-Val-Val-Tyr-Gly-Leu-Arg

SVVYGLR

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Hamada Y, et al. Osteopontin-derived peptide SVVYGLR induces angiogenesis in vivo. Dent Mater J. 2004;23(4):650-655.  [Content Brief]

  [2]. Egusa H, et al. Enhanced bone regeneration via multimodal actions of synthetic peptide SVVYGLR on osteoprogenitors and osteoclasts. Biomaterials. 2009;30(27):4676-4686.  [Content Brief]

  [3]. Uchinaka A, et al. Evaluation of dermal wound healing activity of synthetic peptide SVVYGLR. Biochem Biophys Res Commun. 2017;491(3):714-720.  [Content Brief]