cpt 1

Etomoxir sodium salt ((R)-Etomoxir sodium salt) is a carnitine palmitoyltransferase 1a (CPT-1a) inhibitor that inhibits fatty acid oxidation (FAO). Etomoxir sodium salt has antitumor activity.

Etomoxir is a carnitine palmitoyltransferase 1a (CPT-1a) inhibitor that inhibits fatty acid oxidation by inhibiting CPT-1a and inhibits palmitate oxidation in humans, rats, and guinea pigs. Etomoxir 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.

Irinotecan hydrochloride trihydrate (CPT-11 HCl Trihydrate) keeps DNA from unwinding by inhibiting topoisomerase 1.

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.

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]

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].

1. 7-Ethylcamptothecin has the superior antitumor activity than CPT. (a). 7-Ethylcamptothecin has a stronger growth-inhibiting activity against tumor cells. (b). 7-Ethylcamptothecin remains in the intestinal tract for a longer time and in higher amounts when administered in vivo.

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].

RPR132595A (NPC) hydrochloride, an active metabolite of CPT-11, is produced via cytochrome P-450 3A4 (CYP3A4) metabolism and is ultimately eliminated via urinary excretion [1].

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].

TLR3-IN-1 (CU CPT 4a) is a selective TLR3 inhibitor (IC50: 3.44 μM in RAW 264.7 cells). It can inhibit TLR3 dsRNA complex-mediated downstream signaling pathways and inhibit the production of TNF-α and IL-1β in whole cells.

Perhexiline maleate is an orally active inhibitor of CPT1 and CPT2, reducing fatty acid metabolism, with IC50 values of 77 μM and 148 μM against rat heart and liver CPT1, respectively.

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.

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].

Antitumor Agent-63 (Compound 40), a 20 (S)-O-linked camptothecin (CPT) glycoconjugate, serves as a non-toxic antitumor agent showing high stability and very weak direct inhibition of topoisomerase I (Topo I) [1], demonstrating selective action without harming normal cells.

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-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].

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].

ZBH-1205 is a novel camptothecin derivative, revealing potent antitumor activities mainly through cell apoptosis pathway, being more effective than cpt-11 and sn38 at inhibiting topoismerase-1

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].

A011, a potent and selective ataxia-telangiectasia mutated (ATM) inhibitor, exhibits an IC50 of 1.0 nM and triggers apoptosis as well as G2 M phase cell cycle arrest when combined with CPT-11, displaying notable antitumor activity [1].

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).