Almestrone (developmental code names Ba 38372, Ciba 38372), also known as 7α-methylestrone, is a synthetic, steroidal estrogen which was synthesized in 1967 but was never marketed. It is used as a precursor in the synthesis of several highly active steroi
cvxIAA is an orthogonal auxin-TIR1 receptor pair. cvxIAA triggers auxin signaling without interfering with endogenous auxin or TIR1 AFBs. cvxIAA hijacked the downstream auxin signaling in vivo both at the transcriptomic level and in specific developmental
Fenobucarb, a widely employed carbamate insecticide, poses potential risks to the cardiovascular and cerebrovascular systems in animals[1][2]. It triggers developmental neurotoxicity in zebrafish by engaging pathways related to inflammation, oxidative stress, degeneration, and apoptosis.
Sphingosines are long-chain base precursors of cellular sphingolipids used directly in the synthesis of ceramide, which in combination with sialic acid forms ganglioside. Sphingosine can exist in four stereoisomers, however only sphingosine occurs naturally. Compared to other sphingolipids throughout the body, which are predominantly composed of C-18 sphingosine, only central nervous system (CNS) gangliosides contain significant amounts of sphingosine. The concentration of sphingosine within mammalian brain gangliosides apparently increases with developmental maturation. Furthermore, the ratio of C-18 to C-20 sphingosine in the brain is thought to be related to some nervous system degeneration processes.
Purfalcamine is an orally active, selective Plasmodium falciparum calcium-dependent protein kinase 1 (PfCDPK1) inhibitor with an IC50 of 17 nM and an EC50 of 230 nM. Purfalcamine has antimalarial activity and causes malaria parasites developmental arrest at the schizont stage[1][2]. Purfalcamine has low activity against Toxoplasma gondii calcium-dependent protein kinase 3 (TgCDPK3)[1]. Purfalcamine (225, 450 nM) has no effect on the parasitemia in the first 32 hours. After about 40 hours, parasite level remains stable and then begins dropping[1]. Purfalcamine inhibits proliferation with EC50s of 171-259 nM for P. falciparum strains (3D7, Dd2, FCB, HB3 and W2), which indicates effectiveness against drug-resistant parasites[1]. Given that the EC50 value for P. falciparum (3D7) is 230 nM, Purfalcamine shows a therapeutic window ranging from 23-fold to 36-fold (EC50s for CHO=12.33 μM, HEp2=7.235 μM, HeLa=7.029 μM and Huh7=5.476 μM)[1]. Purfalcamine (10 mg kg; oral gavage; BID; for 6 days) demonstrates a delay in the onset of parasitemia in treated mice[1]. Purfalcamine (20 mg kg; orally gavage) exhibits a Cmax of 2.6 μM with a half-life of 3.1 hours[1]. Animal Model: Male BALB c mice, 7 weeks of age with the malaria parasite[1] [1]. Nobutaka Kato, et al. Gene expression signatures and small-molecule compounds link a protein kinase to Plasmodium falciparum motility. Nat Chem Biol. 2008 Jun;4(6):347-56. [2]. Rajshekhar Y Gaji, et al. Expression of the essential Kinase PfCDPK1 from Plasmodium falciparum in Toxoplasma gondii facilitates the discovery of novel antimalarial drugs. Antimicrob Agents Chemother. 2014 May;58(5):2598-607.
Thalidomide-piperazine hydrochloride is a chemical compound with potential applications in the research of leprosy and multiple myeloma. It serves as a valuable tool in developmental biology, facilitating significant discoveries in the biochemical pathways of limb development [1].