CT-1 

CT-1 is a secreted protein belonging to the IL-6 cytokine family. Overexpression of CT-1 enhances cell proliferation, migration and angiogenesis via the ADMA/DDAH pathway. CT-1 inhibits the growth of triple-negative breast cancer cells by simultaneously inducing Ferroptosis in N2-type tumor-associated neutrophils and cancer cells. CT-1 activates the Jak/STAT-3, p42/p44 MAPK and AMPK pathways, and inhibits GSK-3β activity through phosphorylation to induce cardiomyocyte hypertrophy. CT-1 enhances the viability of cardiomyocytes and neurons, reduces cell Apoptosis, induces the expression of heat shock proteins (HSP) and BNP, and inhibits TNF levels. CT-1 exerts anti-tumor activity in mouse models of triple-negative breast cancer. CT-1 improves cognitive impairment in mice. CT-1 is applicable to the research of ischemic heart disease, triple-negative breast cancer, myocardial hypertrophy, Parkinson's disease, hypertensive heart disease, myocardial infarction, acute Chagas cardiomyopathy, high-fat diet-induced cognitive impairment and diabetes-related cognitive impairment^{[1][2][3][4][5]}.

Overexpression of CT-1 (48 h post-transfection) significantly promotes the proliferation and migration of HUVECs, enhances the capillary-like tube formation ability of cells, significantly upregulates the expression of eNOS mRNA, and increases the protein expression levels of DDAH I, DDAH II and VEGF^[1].
Overexpression of CT-1 (48 h post-transfection) significantly reduces the level of ADMA in HUVECs, enhances DDAH activity, and increases NOS activity and NO production^[1].
CT-1 (0.78-12.5 μM; 0-300 s) binds to purified human FTH1 and wild-type FTH1, with K_d values of 17.15 μM and 5.46 μM, respectively^[2].
CT-1 (100 μM at room temperature; 1 h) interacts with FTH1 in 4T1 cell lysates and reduces the stability of FTH1 against pronase-mediated proteolysis^[2].
CT-1 (0.5-16 μM; 24 h) inhibits the viability of 4T1, MDA-MB-231, and N2-type tumor-associated neutrophils (polarized HL-60 cells) in a dose-dependent manner^[2].
CT-1 (24 h) inhibits the viability of primary mouse N2-like neutrophils with an IC₅₀ of 7.16 μM^[2].
CT-1 (0-8 μM; 24 h) increases intracellular Fe²⁺ levels and the GSSG/GSH ratio (a marker of oxidative stress), reduces mitochondrial membrane potential, promotes intracellular ROS production, induces cellular lipid peroxidation, and facilitates lysosomal autophagic degradation of FTH1 in 4T1 cells^[2].
CT-1 (1-4 μM; 24 h) induces lipid peroxidation in N2-type tumor-associated neutrophils (polarized HL-60 cells)^[2].
CT-1 (0.25-32 μM; 6 days) inhibits the growth and viability of triple-negative breast cancer organoids in a dose-dependent manner, with IC₅₀ values ranging from 2.35 to 6.74 μM across 3 PDO cell lines after 6 days of treatment^[2].
CT-1 (0.1 nM or lower) potently induces volume overload-like hypertrophy in neonatal cardiomyocytes, enhances the survival rate of neonatal rat cardiomyocytes in serum-free medium by reducing apoptosis, and upregulates the expression of ANP, BNP, hsp70 and hsp90 genes in cultured cardiomyocytes^[3].
CT-1 (30 min) protects neonatal cardiomyocytes cultured in vitro from cell death and apoptosis induced by simulated hypoxia/ischemia stress, and this effect depends on the activation of the p42/p44 MAPK pathway (which can be inhibited by 50 μM PD98059 (HY-12028))^[3].

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

CT-1 (i.v., once daily for 14 consecutive days, 5-10 mg/kg) induces ferroptosis in the EMT6 triple-negative breast cancer mouse model, significantly reduces tumor weight, upregulates the levels of oxidative stress and lipid peroxidation markers, and downregulates the expression of the ferroptosis inhibitory proteins FTH1 and GPX4. Its antitumor efficacy against orthotopic 4T1 triple-negative breast cancer tumors decreases under neutrophil-depleted conditions^[2].
CT-1 (1 μg/day; i.c.v.; daily administration for 14 consecutive days) improves cognitive impairment in male C57BL/6 mice induced by a high-fat diet by reversing metabolic dysfunction, alleviating neuroinflammation, enhancing the hippocampal insulin/IGF signaling pathway, and restoring synaptic protein levels. It also ameliorates cognitive deficits, mitochondrial dysfunction, synaptic loss, and insulin signaling pathway defects in mice treated with ICV-Streptozotocin (STZ) (HY-13753) via activating AMPK^[4].

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

394.42

C₂₃H₂₂O₆

Solid

Light yellow to yellow

O=C(C1(C)C)C=CC2=C1C=CC3=C2C(OC(C)=O)=C(OC(C)=O)C4=C3OC[C@@H]4C

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture and light

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Zheng ZZ, et al. CT-1 induces angiogenesis by regulating the ADMA/DDAH Pathway. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2015;159(4):540-546.  [Content Brief]

  [2]. Liu Y, et al. Dual ferroptosis induction in N2-TANs and TNBC cells via FTH1 targeting: A therapeutic strategy for triple-negative breast cancer. Cell Rep Med. 2025;6(1):101915.  [Content Brief]

  [3]. Latchman DS. Cardiotrophin-1 (CT-1): a novel hypertrophic and cardioprotective agent. Int J Exp Pathol. 1999 Aug;80(4):189-96.  [Content Brief]

  [4]. Wang D, et al. Cardiotrophin-1 (CT-1) improves high fat diet-induced cognitive deficits in mice. Neurochem Res. 2015;40(4):843-853.  [Content Brief]

  [5]. Wang D, et al. Treatment effects of Cardiotrophin-1 (CT-1) on streptozotocin-induced memory deficits in mice. Exp Gerontol. 2017;92:42-45.  [Content Brief]