Endotrophin (Mus musculus) TFA 

Endotrophin (Mus musculus) TFA is an adipokine, a cleavage fragment derived from Collagen VI, whose levels are elevated in adipose tissue and breast tumors of obese mice. Endotrophin (Mus musculus) TFA activates the TGF-β signaling pathway and reduces the expression of hormone-sensitive lipase. Endotrophin (Mus musculus) TFA induces adipogenesis, lipid accumulation, fibrosis, inflammation, angiogenesis, adipose tissue expansion, epithelial-mesenchymal transition, and insulin resistance; it also induces Cisplatin (HY-17394) resistance in cancer cells. Endotrophin (Mus musculus) TFA can be used in research related to metabolic diseases such as obesity and type 2 diabetes, as well as cancers such as breast cancer^[1][2][3].

Endotrophin (Mus musculus) (24 h) TFA upregulates the expression of pro-fibrotic (Col1α1, Tgfβ1, TgfβR2) and pro-inflammatory (Nlrp3, Tlr4) genes in the stromal vascular fraction (SVF) isolated from mouse white adipose tissue (WAT)^[1].
Endotrophin (Mus musculus) (24-72 h) TFA induces fibrosis in differentiating 3T3-L1 mouse adipocytes, reduces adiponectin expression, promotes adipogenesis, inhibits lipolysis, and increases lipid accumulation^[1].
Endotrophin (Mus musculus) (24 h) TFA upregulates the expression of Lox, pro-inflammatory genes (Il-1β, Tnf-α, F4/80), and M1 macrophage markers (Cd40, Cd86) in primary macrophages isolated from mouse white adipose tissue (WAT)^[1].
Endotrophin (Mus musculus) TFA is abundantly secreted in fully differentiated 3T3-L1 adipocytes, whereas no secreted level is detected in 3T3-L1 preadipocytes^[3].

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

Endotrophin (Mus musculus) (200 mg/kg; ad libitum; 8 weeks) TFA administration in high-fat diet-fed mice induces local adipose tissue overexpression that promotes adipogenesis, suppresses lipolysis via reduced HSL phosphorylation, enhances lipid accumulation in adipose tissue, and shifts macrophage polarization toward a pro-inflammatory M1 phenotype^[1].
Neutralizing antibody against Endotrophin (Mus musculus) TFA neutralizes endotrophin activity in high-fat diet-induced obese mice and significantly improves insulin sensitivity^[2].
Overexpression of Endotrophin (Mus musculus) TFA in MMTV-PyMT transgenic mice significantly increases primary tumor volume, promotes the growth of lung metastatic lesions, and restores tumor growth in collagen VI-deficient MMTV-PyMT mice^[2].
Induction of Endotrophin (Mus musculus) TFA confers cisplatin resistance in breast tumor-bearing mice, while neutralizing Endotrophin activity or reducing its levels using TZDs restores cisplatin sensitivity^[2].
Endotrophin (Mus musculus) TFA induces adipose tissue fibrosis and inflammation in mice, and causes systemic dyslipidemia, hepatic steatosis and insulin resistance; blocking endogenous Endotrophin with neutralizing antibodies effectively reverses these manifestations^[3].

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

7876.83 (free acid)

C₃₄₅H₅₂₀N₉₂O₁₀₆S₇.xC₂HF₃O₂

Thr-Glu-Pro-Leu-Phe-Leu-Thr-Lys-Thr-Asp-Ile-Cys-Lys-Leu-Ser-Arg-Asp-Ala-Gly-Thr-Cys-Val-Asp-Phe-Lys-Leu-Leu-Trp-His-Tyr-Asp-Leu-Glu-Ser-Lys-Ser-Cys-Lys-Arg-Phe-Trp-Tyr-Gly-Gly-Cys-Gly-Gly-Asn-Glu-Asn-Arg-Phe-His-Ser-Gln-Glu-Glu-Cys-Glu-Lys-Met-Cys-Ser-Pro-Glu-Leu-Thr-Val (Disulfide bridge:Cys12-Cys62,Cys21-Cys4,Cys37-Cys58)

TEPLFLTKTDICKLSRDAGTCVDFKLLWHYDLESKSCKRFWYGGCGGNENRFHSQEECEKMCSPELTV (Disulfide bridge:Cys12-Cys62,Cys21-Cys4,Cys37-Cys58)

O=C(N[C@@H](CCC(O)=O)C(N1[C@@H](CCC1)C(N[C@@H](CC(C)C)C(N[C@@H](CC2=CC=CC=C2)C(N[C@@H](CC(C)C)C(N[C@@H]([C@H](O)C)C(N[C@@H](CCCCN)C(N[C@@H]([C@H](O)C)C(N[C@@H](CC(O)=O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CSSC[C@@H](C(N[C@@H](CO)C(N3[C@@H](CCC3)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC(C)C)C(N[C@@H]([C@H](O)C)C(N[C@@H](C(C)C)C(O)=O)=O)=O)=O)=O)=O)=O)NC4=O)C(N[C@@H](CCCCN)C(N[C@@H](CC(C)C)C(N[C@@H](CO)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC(O)=O)C(N[C@@H](C)C(NCC(N[C@@H]([C@H](O)C)C(N[C@@H](CSSC[C@@H](C(NCC(NCC(N[C@@H](CC(N)=O)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC(N)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC5=CC=CC=C5)C(N[C@@H](CC6=CNC=N6)C(N[C@@H](CO)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCC(O)=O)C(N[C@H]7CCC(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)NC8=O)C(N[C@@H](C(C)C)C(N[C@@H](CC(O)=O)C(N[C@@H](CC9=CC=CC=C9)C(N[C@@H](CCCCN)C(N[C@@H](CC(C)C)C(N[C@@H](CC(C)C)C(N[C@@H](CC%10=CNC%11=CC=CC=C%10%11)C(N[C@@H](CC%12=CNC=N%12)C(N[C@@H](CC%13=CC=C(C=C%13)O)C(N[C@@H](CC(O)=O)C(N[C@@H](CC(C)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CO)C(N[C@@H](CCCCN)C(N[C@@H](CO)C(N[C@@H](CSSC[C@@H](C(N[C@@H](CCC(O)=O)C(N[C@@H](CCCCN)C(N[C@H]4CCSC)=O)=O)=O)NC7=O)C(N[C@@H](CCCCN)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC%14=CC=CC=C%14)C(N[C@@H](CC%15=CNC%16=CC=CC=C%15%16)C(N[C@@H](CC%17=CC=C(C=C%17)O)C(NCC(NC8)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H]([C@H](O)C)N.OC(C(F)(F)F)=O.[x]

Room temperature in continental US; may vary elsewhere.

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

• [1]. Zhao Y, et al. Divergent functions of endotrophin on different cell populations in adipose tissue. Am J Physiol Endocrinol Metab. 2016;311(6):E952-E963.  [Content Brief]

  [2]. Sun K, et al. Endotrophin, a multifaceted player in metabolic dysregulation and cancer progression, is a predictive biomarker for the response to PPARγ agonist treatment. Diabetologia. 2017;60(1):24-29.

  [3]. Sun K, et al. Endotrophin triggers adipose tissue fibrosis and metabolic dysfunction. Nat Commun. 2014;5:3485. Published 2014 Mar 19.