cpt

8-Cyclopentyl-1,3-dimethylxanthine (CPT) is a potent antagonist of adenosine A1 receptor.

9-Oxononanoic Acid is an oxidized fatty acid, formed by the autoxidation of linoleic acid, which enhances phospholipase A2 (PLA2) activity and increases the production of thromboxane B2 in isolated human plasma.9-Oxononanoic Acid reduces hepatic neofatty acid synthesis and enhances the activity of rat hepatic carnitine palmitoyltransferase, a marker of β-oxidation. Activity.

Camptothecin (CPT) belongs to the alkaloid group of natural products and is a specific DNA topoisomerase I (Topo I) inhibitor (IC50=679 nM) with specificity. Camptothecin has antitumor activity and induces apoptosis.

CU-CPT17e is a potent agonist of TLR(TLR3, TLR8, and TLR9).

CU-CPT22 is the first probe for the complex between toll-like receptors TLR1 and TLR2. CU-CPT22 binds at the interface of TLR1 and TLR2 (IC50 = 0.58 μM). It competes with the synthetic triacylated lipoprotein (Pam3CSK4) binding to TLR1/2 (Ki: 0.41 μM).

8-CPT-cAMP is a PDE Va inhibitor.

iRGD–CPT is an iRGD-camptothecin conjugate covalently linked via a heterobifunctional linker. It exhibits anticancer activity both in vivo and in vitro and can be utilized in colon cancer research.

(GalNAc)3-CPT is a glycan-conjugated prodrug that targets the asialoglycoprotein receptor (ASGR) overexpressed on liver cells. It demonstrates significant antitumor activity by activating the cGAS-STING pathway and promoting CD8+ T cell infiltration into tumor sites, leading to apoptosis of tumor cells. In HepG2 cells, it shows an IC50 value of 3.07 μM.

8-CPT-Cyclic AMP sodium is an activator of cAMP-dependent PKA and cAMP receptor activator, and also an inhibitor of cAMP-specific phosphodiesterase (PDE VA) (IC50 = 0.9 μM). The IC50 values for PDE III and PDE IV are 24 and 25 μM, respectively.

8-CPT-2Me-cAMP sodium is a sodium salt compound that selectively activates exchange proteins activated by cAMP (Epac), which are cAMP-sensitive guanine nucleotide exchange factors (GEFs) responsible for activating small GTPases Rap1 and Rap2. It specifically activates Epac1 with an EC50 value of 2.2 μM, while showing no activation of PKA with an EC50 value greater than 10 μM [1]. Additionally, 8-CPT-2Me-cAMP sodium stimulates the Epac-mediated release of calcium ions (Ca2+) in vitro in pancreatic β-cells [2].

Rp-8-CPT-cAMP is a structural combination of the lipophilic and non-hydrolyzable cAMP analogs, 8-CPT-cyclic AMP and Rp-cyclic AMPS .[1] It functions as a site-selective inhibitor of protein kinase A (PKA) type I and II, with preference towards site A of type I and site B of type II.2 By occupying cAMP binding sites at the regulatory subunit of PKA, Rp-8-CPT-cAMP prevents the kinase holoenzyme from dissociative activation.[2],[3]

Sp-8-CPT-cAMPS is a powerful and specific cAMP analog that activates cAMP-dependent protein kinase A (PKA I and PKA II) selectively and effectively. It exhibits a 153-fold preference for site A of RI over site A of RII, and a 59-fold preference for site B of RII over site B of RI.

Rp-8-CPT-cAMPS is a powerful and competitive antagonist of cAMP-induced activation of cAMP-dependent protein kinase (PKA) I and II. Acting as a potent cAMP analog, Rp-8-CPT-cAMPS exhibits a preference for site A of RI over site A of RII. Additionally, it favors site B of RII over site B of RI. This compound effectively inhibits cAMP-dependent PKA activation and demonstrates selectivity in binding to specific sites within the protein kinase.

CPT-157633 is a difluoro-phosphonomethyl phenylalanine derivative that acts as a potent inhibitor of the enzyme PTP1B. It effectively prevents the development of glucose intolerance induced by binge drinking.

CU-CPT9b (TLR8-specific antagonist 1) is an antagonist of toll-like receptor 8 (TLR8; Kd = 21 nM). It inhibits activation of NF- B induced by the TLR8 agonist R-848 in TLR8-overexpressing HEK-Blue cells with an IC50 value of 0.7 nM.

CU-CPT-9a is a potent TLR8 inhibitor (IC50 : 0.5 nM), that suppresses TLR8-mediated proinflammatory signaling in various cell lines and human primary cells-

CPT-Se3, a camptothecin (CPT) seleno-derivative, exhibits enhanced anticancer efficacy by effectively killing cancer cells and hindering tumor proliferation. This compound diminishes the GSH/GSSG ratio and total thiols while increasing ROS levels, ultimately triggering apoptosis in Hep G2 cells. Furthermore, CPT-Se3 demonstrates significant cytotoxicity against HeLa, Hep G2, A549, and SMMC-7721 cell lines with IC50 values ranging from 2.19 to 4.7 μM [1].

CPT-Se4, a seleno-derivative of Camptothecin (CPT), exhibits enhanced efficacy in cancer cell eradication and tumor suppression. It reduces the GSH/GSSG balance and total thiol content while increasing ROS concentrations in Hep G2 cells, leading to the induction of cancer cell apoptosis. Furthermore, CPT-Se4 demonstrates cytotoxicity towards a range of cell lines including HeLa, Hep G2, A549, and SMMC-7721, with IC50 values ranging from 2.54 to 6.4 μM [1].

CU-CPT-8m (TLR8-specific antagonist) is an toll-like receptor 8 (TLR8) antagonist (IC50 : 67 nM)

8-CPT-6-Phe-cAMP is a potent analog of the signaling molecule cAMP and a powerful activator of protein kinase A (PKA).

8-CPT-2'-O-Me-cAMP (250 µM; 1 h) induces Rap1 activation and enhances the recruitment of junction proteins and cortical F-actin in retinal pigment epithelial cells.

8-CPT-cAMP-AM is a highly membrane-permeable analog of the signaling molecule cAMP. It serves as an activator for both cAMP and cGMP-dependent protein kinases, as well as Epac (exchange protein activated by cAMP).

Etomoxir is an irreversible inhibitor of carnitine palmitoyltransferase 1a (CPT-1a) (IC50=5-20 nM). Etomoxir inhibits fatty acid oxidation by inhibiting CPT-1a, inhibits palmitate oxidation, has an inhibitory effect on adenine nucleotide translocase, and can inhibit macrophage polarization by disrupting CoA homeostasis.

McN3716 is a carnitine palmitoyltransferase I (CPT-1) inhibitor used for researching metabolic diseases.