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Dimethandrolone Undecanoate (DMAU) is a novel orally available androgen with progestational activity and is a potential male contraceptive compound.

Handle region peptide, rat acetate is a prorenin receptor antagonist, suppresses the progression of diabetic nephropathy and has anti-inflammatory in the eye.

Glycerol or glycerin is a colourless, odourless, viscous liquid that is sweet-tasting and mostly non-toxic. It is widely used in the food industry as a sweetener and humectant and in pharmaceutical formulations. Glycerol is an important component of trigl

Handle region peptide, rat, functions as a prorenin receptor antagonist, effectively inhibiting the development of diabetic nephropathy while also exhibiting anti-inflammatory properties specifically within the eye.

Isochandalone is a natural product from Derris robusta.

CALP2 acetate is an antagonist of calmodulin showing high affinity for binding to the CaM EF-hand/Ca2+-binding site with a Kd of 7.9 µM. CALP2 acetate potently inhibits of adhesion and degranulation. CALP2 acetate is also a strong activator of alveolar macrophages. CALP2 acetate inhibits CaM-dependent phosphodiesterase activity and increases intracellular Ca2+ concentrations.

CALP1 acetate is a calmodulin (CaM) agonist (Kd of 88 µM) that binds to the CaM EF-hand/Ca2+-binding site. CALP1 blocks calcium influx and apoptosis (IC50 of 44.78 µM) by inhibiting the open of calcium channel. CALP1 blocks glutamate receptor channels and blocks a store-operated nonselective cation channel. CALP1 activates CaM-dependent phosphodiesterase activity.

CALP3 acetate is a potent Ca2+ channel blocker that activates EF hand motifs of Ca2+-binding proteins. CALP3 acetate can functionally mimic increased [Ca2+]i by modulating the activity of Calmodulin (CaM), Ca2+ channels and pumps.

Methandienone-d3 is a deuterated compound of Methandienone.

Handelin has anti-inflammatory activity by inhibiting NF-κB activation and pro-inflammatory cytokine productions.

Sahandol shows antiprotozoal activity against P. falciparum and T. brucei rhodesiense.

Cell-permeable calmodulin (CaM) agonist that binds to the EF-hand/Ca2+-binding site. Activates phosphodiesterase in the absence of Ca2+ and inhibits Ca2+-mediated cytotoxicity and apoptosis (IC50 = 33 μM).

Cell-permeable calmodulin (CaM) agonist that binds to the EF-hand/Ca2+-binding site; produces CaM-dependent activation of phosphodiesterase. Also binds to cytoplasmic sites on other Ca2+ channels, including NMDA and HIV-1 gp120-activated channels, inhibit

Tat-NR2BAA is an inactive control peptide of Tat-NR2B9c. It shares a similar sequence with Tat-NR2B9c, but possesses a double-point mutation in the COOH terminal tSXV motif. This mutation renders Tat-NR2BAA unable to bind PSD-95. Tat-NR2B9c, on the other hand, is a membrane-permeable peptide that interferes with PSD-95/NMDAR binding. This interference leads to the decoupling of NR2B- and/or NR2A-type NMDARs from PSD-95[1][2].

ABO acts as an annexin A7 modulator, specifically binding to Thr286 to inhibit its phosphorylation on threonine (not on serine or tyrosine) residues within human umbilical vein endothelial cells (HUVECs). This compound furthers the annexin A7 interaction with the EF-hand protein GCA, leading to reduced GCA phosphorylation, lowered intracellular calcium levels, and enhanced autophagy in COS-7 cells. Moreover, ABO lessens phosphorylation of the microtubule-associated protein 1 light chain (LC3) in HUVECs and impedes the upregulation of phosphatidylcholine-specific phospholipase C (PC-PLC) due to oxidized low-density lipoprotein in vascular endothelial cells (VECs). In animal models, specifically apoE-/- mice on a Western diet, administration of ABO (50 or 100 mg/kg per day) has been shown to decrease PC-PLC expression, promote autophagy, and reduce apoptosis, lipid accumulation, and the extent of atherosclerotic plaques in the aortic endothelium.

Trioxsalen (Trioxysalen) is a furanocoumarin and a psoralen derivative, in conjunction with UV-A for phototherapy treatment of vitiligo and hand eczema. After photoactivation it creates interstrand cross-links in DNA, which can cause programmed cell death.

CALP3 TFA is a potent Ca2+ channel blocker that activates EF-hand motifs of Ca2+-binding proteins. It can functionally mimic increased [Ca2+]i by modulating the activity of Calmodulin, Ca2+ channels, and pumps.

CALP2 TFA, a potent calmodulin (CaM) antagonist with a dissociation constant (Kd) of 7.9 µM, exhibits high affinity for the CaM EF-hand/Ca2+-binding site. This compound effectively inhibits CaM-dependent phosphodiesterase activity and elevates intracellular Ca2+ concentrations. Furthermore, it significantly hinders adhesion and degranulation, while also acting as a robust activator of alveolar macrophages [1] [2] [3] [4].

CALP3 TFA, a Ca2+-like peptide and potent Ca2+ channel blocker, activates EF hand motifs in Ca2+-binding proteins. It can mimic increased [Ca2+]i, modulating the activity of Calmodulin (CaM), Ca2+ channels, and pumps. This compound shows promise in controlling apoptosis in conditions like AIDS or ischemic neuronal loss [1] [2].

Nematocyphol is a triterpenoid from Euphorbia nematocypha hand-mazz.

Cell-permeable calmodulin (CaM) antagonist that binds to the EF-hand/Ca2+-binding site. CALP2 has been demonstrated to inhibit CaM-dependant phosphodiesterase activity and increase intracellular Ca2+ concentrations by modulating Ca2+-channel activity. CAL

3-Hydroxybutyric acid (Butanoic acid) (or beta-hydroxybutyrate) is a ketone body. Like the other ketone bodies (acetoacetate and acetone), levels of 3-hydroxybutyrate in blood and urine are raised in ketosis. In humans, 3-hydroxybutyrate is synthesized in the liver from acetyl-CoA and can be used as an energy source by the brain when blood glucose is low. Blood levels of 3-hydroxybutyric acid levels may be monitored in diabetic patients to look for diabetic ketoacidosis. Persistent mild hyperketonemia is a common finding in newborns. Ketone bodies serve as an indispensable source of energy for extrahepatic tissues, especially the brain and lung of developing mammals. Another important function of ketone bodies is to provide acetoacetyl-CoA and acetyl-CoA for the synthesis of cholesterol, fatty acids, and complex lipids. During the early postnatal period, acetoacetate (AcAc) and beta-hydroxybutyrate are preferred over glucose as substrates for synthesis of phospholipids and sphingolipids in accord with requirements for brain growth and myelination. Thus, during the first 2 weeks of postnatal development, when the accumulation of cholesterol and phospholipids accelerates, the proportion of ketone bodies incorporated into these lipids increases. On the other hand, an increased proportion of ketone bodies is utilized for cerebroside synthesis during the period of active myelination. In the lung, AcAc serves better than glucose as a precursor for the synthesis of lung phospholipids. The synthesized lipids, particularly dipalmitoylphosphatidylcholine, are incorporated into surfactant, and thus have a potential role in supplying adequate surfactant lipids to maintain lung function during the early days of life (PMID: 3884391 ). 3-Hydroxybutyric acid is found to be associated with fumarase deficiency and medium-chain acyl-CoA dehydrogenase deficiency, which are inborn errors of metabolism.

CALP1 TFA, a calmodulin (CaM) agonist with a dissociation constant (Kd) of 88 µM, selectively binds to the CaM EF-hand/Ca2+-binding site, inhibiting calcium channel opening. This action blocks calcium influx and apoptosis with an IC50 of 44.78 µM, modulates glutamate receptor channel activity, and impedes a store-operated nonselective cation channel. Additionally, CALP1 TFA enhances CaM-dependent phosphodiesterase activity, denoting its multifaceted role in modulating cellular calcium dynamics [1] [2] [3] [4].

Tinoridine hydrochloride (Y-3642 hydrochloride) is a non-steroidal anti-inflammatory drug. Tinoridine hydrochloride (5-100 μM), produced a concentration-dependent inhibition on the simultaneous increases in lipid peroxide formation and renin release induced by 50 μM ascorbic acid in the renin granule fraction. On the other hand, indomethacin, hydrocortisone, and prednisolone, which had no ability to inhibit the lipid peroxidation in the renin granule fraction, did not influence the release of renin from the granules. These results suggest that tinoridine suppresses renin release by inhibiting the oxidative disintegration of membranes of renin granules.