1mg

Molecular Formula : C30H14D18Cl3NO

Molecular Formula : C30H23D9Cl3NO

Molecular Formula : C28 H37 F O7

Molecular Formula : C25 H34 O6

Molecular Formula : C12H2D8N4O2

Molecular Formula : C21 H21 Cl F N O8

Molecular Formula : C28H44O

Molecular Formula : C27 H44 O

Molecular Formula : C30H47D3O

Molecular Formula : C20 H18 O5

Molecular Formula : C28H28D8N4O2S HCl

Molecular Formula : C15 H12 F N3 O5 S

Molecular Formula : C21H19Cl2N5O2

Molecular Formula : C17 H12 N4

Molecular Formula : C20 H21 N5 O7

Molecular Formula : C29H30D8N4O10

Molecular Formula : C20 H25 N3 O

Molecular Formula : C20 D3 H22 N3 O

Molecular Formula : C12 H25 N3 O4

Molecular Formula : C46H63D2N13O12S2 . x(C 2HF3O2)

Molecular Formula : C46H60D5N13O12S2 • x(C2HF3O2)

Molecular Formula : C9 D2 H6 Cl 15N O3

Macrophage-Colony Stimulating Factor (M-CSF), also known as Colony Stimulating Factor-1 (CSF-1), is a hematopoietic growth factor. It can stimulate the survival, proliferation and differentiation of mononuclear phagocytes, in addition to the spreading and motility of macrophages. In mammals, it exits three isoforms, which invariably share an N-terminal 32-aa signal peptide, a 149-residue growth factor domain, a 21-residue transmembrane region and a 37-aa cytoplasmictail. M-CSF is mainly produced by monocytes, macrophages, fibroblasts, and endothelial cells. M-CSF interaction with its receptor, c-fms, has been implicated in the growth, invasion, and metastasis of of several diseases, including breast and endometrial cancers. The biological activity of human M-CSF is maintained within the 149-aa growth factor domain, and it is only active in the disulfide-linked dimeric form, which is bonded at Cys63.

Macrophage-Colony Stimulating Factor (M-CSF), also known as Colony Stimulating Factor-1 (CSF-1), is a hematopoietic growth factor. It can stimulate the survival, proliferation and differentiation of mononuclear phagocytes, in addition to the spreading and motility of macrophages. In mammals, it exits three isoforms, which invariably share an N-terminal 32-aa signal peptide, a 149-residue growth factor domain, a 21-residue transmembrane region and a 37-aa cytoplasmictail. M-CSF is mainly produced by monocytes, macrophages, fibroblasts, and endothelial cells. M-CSF interaction with its receptor, c-fms, has been implicated in the growth, invasion, and metastasis of of several diseases, including breast and endometrial cancers. The biological activity of human M-CSF is maintained within the 149-aa growth factor domain, and it is only active in the disulfide-linked dimeric form, which is bonded at Cys63.

Macrophage-Colony Stimulating Factor (M-CSF), also known as Colony Stimulating Factor-1 (CSF-1), is a hematopoietic growth factor. It can stimulate the survival, proliferation and differentiation of mononuclear phagocytes, in addition to the spreading and motility of macrophages. In mammals, it exits three isoforms, which invariably share an N-terminal 32-aa signal peptide, a 149-residue growth factor domain, a 21-residue transmembrane region and a 37-aa cytoplasmictail. M-CSF is mainly produced by monocytes, macrophages, fibroblasts, and endothelial cells. M-CSF interaction with its receptor, c-fms, has been implicated in the growth, invasion, and metastasis of of several diseases, including breast and endometrial cancers. The biological activity of human M-CSF is maintained within the 149-aa growth factor domain, and it is only active in the disulfide-linked dimeric form, which is bonded at Cys63.

Macrophage-Colony Stimulating Factor (M-CSF), also known as Colony Stimulating Factor-1 (CSF-1), is a hematopoietic growth factor. It can stimulate the survival, proliferation and differentiation of mononuclear phagocytes, in addition to the spreading and motility of macrophages. In mammals, it exits three isoforms, which invariably share an N-terminal 32-aa signal peptide, a 149-residue growth factor domain, a 21-residue transmembrane region and a 37-aa cytoplasmictail. M-CSF is mainly produced by monocytes, macrophages, fibroblasts, and endothelial cells. M-CSF interaction with its receptor, c-fms, has been implicated in the growth, invasion, and metastasis of of several diseases, including breast and endometrial cancers. The biological activity of human M-CSF is maintained within the 149-aa growth factor domain, and it is only active in the disulfide-linked dimeric form, which is bonded at Cys63.

Molecular Formula : C17H18D3NO5

Molecular Formula : C713C2H915NO4

Molecular Formula : C11 H12 Cl2 N2 O5

Molecular Formula : C17 H25 N2 O3

Molecular Formula : C13 2H9 H9 Cl F3 N2 O

Molecular Formula : C19H16D4Br2N6O4S

Molecular Formula : C9H18Cl2N2NaO5PS2

Molecular Formula : C42H67NO15

Molecular Formula : C21 H26 O4

Molecular Formula : C10 2H6 H13 O6 P S2

Molecular Formula : C18H27N5O7 . x(C 2HF3O2)

Molecular Formula : ¹³C3H6N2O2

Molecular Formula : C42 H72 O36

Molecular Formula : C24H42O21

Molecular Formula : C23H25ClO12.x(C2HF3O2)

Molecular Formula : 13C8H8O3

Molecular Formula : C23 D4 H18 Cl N O4

Molecular Formula : C14H14D6ClF3N2O • HCl

Molecular Formula : C20H19D5ClN

Molecular Formula : C29D6H35F2N5O

Molecular Formula : C32 H40 N2 O . C6 H8 O7

Mammary serine protease inhibitor (Maspin), also known as serpin B5 is a non-inhibitory serpin that is encoded by the SERPINB5 gene in humans. The protein is expressed predominantly in normal mammary epithelial cells but at significantly reduced levels or absent in most breast carcinomas. As it does not undergo the S (stressed) to R (relaxed) conformational transition characteristic of active serpins, it exhibits no serine protease inhibitory activity. The maspin functions as tumor suppressor, blocking the growth, invasion, and metastatic properties of mammary tumors. This anti-tumor activity is achieved, in part, by the ability of maspin to inhibit angiogenesis and to preferentially promote apoptosis of tumor cells.

Molecular Formula : C70H131N19O15 . x(C 2HF3O2)

Molecular Formula : C20 H22 O6