Cholesterol sulfate is quantitatively the most important known sterol sulfate in human plasma, where it is present in a concentration that overlaps that of the other abundant circulating steroid sulfate, dehydroepiandrosterone (DHEA) sulfate. Cholesterol sulfate is generated in the normal epidermis by cholesterol sulfotransferase but then is desulfated in the outer epidermis as part of a 'cholesterol sulfate cycle' that is a powerful regulator of epidermal metabolism and barrier function. It accumulates in the epidermis in the human genetic disorder X-linked ichthyosis. In XLI, cholesterol sulfate levels exceed 10% of total lipid mass (≈1% of total weight). Cholesterol sulfate is a component of cell membranes where it has a stabilizing role, e.g., protecting erythrocytes from osmotic lysis and regulating sperm capacitation. It is present in platelet membranes where it supports platelet adhesion. Cholesterol sulfate can regulate the activity of serine proteases, e.g., those involved in blood clotting, fibrinolysis, and epidermal cell adhesion. Because of its ability to regulate the activity of selective protein kinase C isoforms and modulate the specificity of phosphatidylinositol 3-kinase, cholesterol sulfate is involved in signal transduction.

Сalpeptin is useful cell-penetrative calpain inhibitor. Calpeptin inhibits the cell growth of ER (estrogen receptor) positive breast cancer cells, such as MCF-7, T-47D, and ZR-75-1 in the presence of Estradiol. Studies in rodent and cell culture models of Parkinson's disease suggest that treatment with calpain inhibitor calpeptin can prevent neuronal death and restore functions. The combination of histone deacetylase inhibitors and calpeptin inhibited the growth of two distinctly different types of breast cancer cells and could have wide clinical applications. Calpeptin is a promising antitumor agent for pancreatic cancer.

β-Amyrin, a pentacyclic triterpenoid compound, that was found in many medicinal plants, including Protium heptaphyllum (Aubl.) Marchand, Catharanthus roseus (L.) G. Don, and Camellia tenuifolia (Hayata) Coh. Stuart. Several studies have reported that β-amyrin shows multiple pharmacological activities, such as the induction of angiogenesis in vascular endothelial cells and anti-inflammatory, antifibrotic, anti-apoptotic, anti-diabetic, anti-hyperlipidemic, and anti-nociceptive activities.

Nomilin is a limonoid/triterpenoid found in citrus fruits that exhibits anti-parasitic, antiviral, anticancer, anti-metastatic, anti-angiogenic, anti-inflammatory, immunomodulatory, anti-obesity, anti-diabetic, and antiviral activities. Nomilin prevents growth of Aedes and suppresses replication of HIV-1 by inhibiting HIV-1 protease. In animal models, nomilin induces phase II enzymes by increasing expression of glutathione-S-transferase and NADPH:Quinone reductase. In animals fed high fat diets, nomilin activates GR5, increases glucose tolerance, and decreases body weight, glucose levels, and insulin levels. In vivo, nomilin increases white blood cell counts and antibody titers but suppresses delayed-type hypersensitivity reactions. In vitro, this compound inhibits cell proliferation, migration, invasion, and capillary tube formation and decreases levels of IL-1β, IL-6, TNF-α, VEGF, NO, and GM-CSF. Additionally, nomilin also inhibits aromatase and cellular proliferation in breast cancer cells. Nomilin also inhibits osteoclastogenesis in vitro by suppression of NFATc1 and MAPK signaling pathways. Nomilin inhibits tumor-specific angiogenesis by downregulating VEGF, NO and proinflammatory cytokine profile and also by inhibiting the activation of MMP-2 and MMP-9.

Piericidin A (also named piericidin A1 in some references) was reported as a new insecticidal metabolite, produced by cultures of the soil-derived actinomycete Streptomyces mobaraensis. Piericidin A resembles coenzyme Q in its overall structure containing a pyridine ring with two adjacent methoxy groups. The most widely recognized biological target of Piericidin A is the mitochondrial electron transport chain protein NADH-ubiquinone reductase (Complex I). Respiratory inhibition by piericidin A can be reversed by the addition of vitamin-K3 (menadione) to the inhibited respiratory chain in mammalian mitochondria. Piericidin A increases ROS production. Piericidin A showed significant cytotoxic activities against several tumor cells, such as mouse leukemia cell line, human colon carcinoma cells and was selectively cytotoxic toward human multiple myeloma cells. Moreover, it was identified as a highly selective antitumor agent with greater selectivity and potency than the comparison standard mitomycin C. Piericidin A aggravates the course of genetically determined tau pathology.

Hypocrellin B (HB), a natural perylenequinone pigment, has been successfully employed in the photodynamic therapy (PDT) in a variety of human cancer cells due to its high singlet oxygen yield. Hypocrellin B exhibits antibacterial, anti-metastatic, and anticancer chemotherapeutic activities. Hypocrellin B inhibits proliferation of Staphylococcus by increasing ROS levels and damaging cell walls. In ovarian cancer cells, this compound induces apoptosis and inhibits cell migration and adhesion under photodynamic stimulation; it also induces tumor regression in animal models of lymphoma. In vitro, hypocrellin B induces DNA strand breakage.

NSC-207895 (XI-006) is a derivative of nitrobenzofuroxan and an anticancer agent with an EC50 of 1 μM. NSC-207895 also upregulated the expression of p53 in MCF-7 cells that led to increased expression of proapoptotic genes including PUMA, BAX, as well as PIG3. Notably, NSC-207895, also called a small-molecule p53 activator, gives rise to MCF-7 cells to experience apoptosis and decrease the viability of cancer cells along with nutlin-3a, which dissociated the MDM2-p53 complex. NSC-207895 is an electrophilic compound that has antitumor and mutagenic activities. NSC-207895 may lead to the damage of DNA that inhibits the growth of tumors.

Panaxatriol is a triterpene sapogenin originally found in species of Panax (ginseng) that exhibits anti-inflammatory, hepatoprotective, anti-arrhythmic, and antioxidative activities. Panaxatriol increases expression of heme oxygenase 1 (HO-1) and activation of Nrf2 signaling in neurons in a PI3K/Akt-dependent manner. Panaxatriol also decreases acetaminophen-induced increases in ALT and TNF-α, preventing liver injury in vivo. Additionally, panaxatriol inhibits Ca2+ channels, decreasing channel open time and open state probability in vitro and displaying anti-arrhythmic potential. Panaxatriol is a tyrosine hydroxylase inducer. It shows neuroprotective and cardioprotective effects in vivo. Panaxatriol enhances antioxidant activity and inhibits mitochondria-mediated apoptosis. Pretreatment with ginseng total saponin, especially panaxatriol, ameliorates I/R-induced myocardial damage and this protection is caused by reducing oxidative stress. Panaxatriol can relieve myelosuppression induced by radiation injury. The abilities of regulating the expression of hemopoietic growth factor GM-CSF and promoting the maturation of bone marrow cells may be responsible for some of these beneficial effects.

Y-26763 is an active metabolite of Y-27152. Y-26763 is the novel K channel opener. It has been found to activate K channels in both cardiac myocytes and in smooth muscle cells from various tissues, suggesting that the compound has a non-specific effect on SUR1 and SUR2 channel subunits. Y-26763 well tolerated in healthy volunteers, and its pharmacologic effects were likely caused by vasodilation, which could make it an effective antihypertensive agent. At doses of 0.5 mg or higher, participants experienced headaches and palpitations, which were probably due to the vasodilatory effects and did not require treatment. Y-26763 partially protected against glycerol-induced acute renal failure. Also, it reduces infarct volume in focal cerebral ischemia in rats.