cpt 2

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.

Carnitine palmitoyltransferase 2 (CPT2), an enzyme involved in fatty acid oxidation, serves as a prognostic biomarker for colorectal cancer (CRC). Overexpression of CPT2 activates phosphorylated p53, enhancing its expression, which in turn suppresses tumor growth and induces apoptosis. Conversely, a deficiency in CPT2 leads to the prevalent hereditary disorder of long-chain fatty acid oxidation in skeletal muscle. Additionally, the downregulation of CPT2 correlates strongly with the advancement of multiple cancers, highlighting its importance in cancer research [1] [2].

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-Cyclic AMP (8-CPT-cAMP) sodium is a selective activator of cyclic AMP-dependent protein kinase (PKA) and a potent inhibitor of cyclic GMP-specific phosphodiesterase (PDE VA) with an inhibitory concentration (IC50) of 0.9 μM. It also inhibits PDE III and PDE IV while significantly activating Epac, demonstrating diverse pharmacological activities [1] [2].

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]

9-amino-CPT (Aminocamptothecin) is an inhibitor of topoisomerase I with potent anticancer activity.

Malonyl CoA serves as a substrate in fatty acid biosynthesis while inhibiting fatty acid oxidation. It also acts as a reversible inhibitor of mitochondrial carnitine palmitoyltransferase (CPT) 1 [1] [2].

Deruxtecan Analog 2 (example 9 P3), a Deruxtecan derivative, serves as an agent-linker conjugate integrating Camptothecin (CPT), a Topo I inhibitor active against colorectal, breast, lung, and ovarian cancers, with a distinct linker. This analog is employed in synthesizing anti-FGFR2 ADC [1].

Camptothecin-20(S)-O-propionate hydrate, the C20-propionate ester of CPT, serves as a potent anticancer agent and functions as a topoisomerase-I inhibitor [1] [2]. This compound is often referenced by its alternate name, Camptothecin-20-O-propionate.

Malonyl CoA tetralithium (Malonyl coenzyme A), serves as a substrate in fatty acid biosynthesis and functions as an inhibitor of fatty acid oxidation. Additionally, it acts as a reversible inhibitor of mitochondrial carnitine palmitoyltransferase (CPT) 1 [1] [2].