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Merck
CN

SML3344

Vosoritide Trifluoroacetate

≥95% (HPLC)

Synonym(s):

BMN 111 Trifluoroacetate, PGQEHPNARK YKGANKKGLS KGCFGLKLDR IGSMSGLGC Trifluoroacetate, cyclic (23→39)-disulfide L-prolylglycyl-L-glutaminyl-L-α-glutamyl-L-histidyl-L-prolyl-L-asparaginyl-L-alanyl-L-arginyl-L-lysyl-L-tyrosyl-L-lysylglycyl-Lalanyl-L-asparaginyl-L-lysyl-L-lysylglycyl-L-leucyl-L-seryl-L-lysylglycyl-L-cysteinyl-L-phenylalanylglycyl-L-leucyl-L-lysyl-L-leucyl-L-α-aspartyl-L-arginyl-L-isoleucylglycyl-L-seryl-L-methionyl-L-serylglycyl-L-leucylglycyl-L-Cysteine Trifluoroacetate

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About This Item

Empirical Formula (Hill Notation):
C176H290N56O51S3 · xC2HF3O2
Molecular Weight:
4102.73 (free base basis)
NACRES:
NA.77
UNSPSC Code:
12352200
Assay:
≥95% (HPLC)
Form:
powder
Quality level:
100

Key Documents

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assay

≥95% (HPLC)

form

powder

color

white to off-white

storage temp.

−20°C

Quality Level

100

Related Categories

Biochem/physiol Actions

More stable analogue of human C-type natriuretic peptide (CNP)
Vosoritide is a more stable analogue of human C-type natriuretic peptide (CNP). Vosoritide binds to the Natriuretic-Peptide Receptor B (NPR B), which leads to MAPK pathway inhibition and an increased production of Extracellular Matrix. It reduces the achondroplastic phenotype. Vosoritide is approved for treatment of Achondroplasia aged 5 and up.

Storage Class

11 - Combustible Solids

wgk

WGK 3

Regulatory Information

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Certificates of Analysis (COA)

Lot/Batch Number
0000180382
0000240538
0000176742
0000180382
0000176742

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Wiktoria Wrobel et al.
International journal of molecular sciences, 22(11) (2021-06-03)
Achondroplasia (ACH) is a disease caused by a missense mutation in the FGFR3 (fibroblast growth factor receptor 3) gene, which is the most common cause of short stature in humans. The treatment of ACH is necessary and urgent because untreated
Florence Lorget et al.
American journal of human genetics, 91(6), 1108-1114 (2012-12-04)
Achondroplasia (ACH), the most common form of dwarfism, is an inherited autosomal-dominant chondrodysplasia caused by a gain-of-function mutation in fibroblast-growth-factor-receptor 3 (FGFR3). C-type natriuretic peptide (CNP) antagonizes FGFR3 downstream signaling by inhibiting the pathway of mitogen-activated protein kinase (MAPK). Here
Leia C Shuhaibar et al.
JCI insight, 6(9) (2021-05-15)
Activating mutations in fibroblast growth factor receptor 3 (FGFR3) and inactivating mutations in the natriuretic peptide receptor 2 (NPR2) guanylyl cyclase both result in decreased production of cyclic GMP in chondrocytes and severe short stature, causing achondroplasia (ACH) and acromesomelic

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