1. Deoxyshikonin (Arnebin 7) may be a new drug candidate for wound healing and treatment of lymphatic diseases. 2. Deoxyshikonin enhances the ability of human dermal lymphatic microvascular endothelial cells (HMVEC-dLy) to undergo time-dependent in vitro cord formation. 3. Deoxyshikonin and dodecyl gallate show significantly synergic antimicrobial activity with penicillin in vivo and in vitro, and can effectively reduce nasopharyngeal and lung colonization caused by different penicillin-resistant pneumococcal serotypes.

Beta-Hydroxyisovalerylshikonin is an inhibitor of protein-tyrosine kinases such as v-Src and EGFR, and has been shown to induce apoptosis in several human tumor cell lines. Beta-Hydroxyisovalerylshikonin significantly decreased viability of HCT116 cells (IC50 values = 30.9 μg/mL).

β,β-Dimethylacrylalkannin is a natural product isolated from Arnebia nobilis Reichb.f, increases collagen and involucrin content in skin cells.

Isobutylshikonin exhibits obvious antioxidant activities , it exerts very good radical scavenging activities toward ABTS+ but shows moderate inhibition of DPPH·.

1. Acetylshikonin exhibits weak cytotoxicity against human umbilical vein endothelial cells (HUVECs) with IC5 of over 2 microM, exhibits the antiangiogenic and antitumorigenic effects by suppressing proliferation and angiogenic factors. 2. Acetylshikonin inhibits the generation of NADPH oxidase complex in the activation of respiratory burst of PMNs, but does not directly inhibit the activity of NADPH oxidase already generated. 3. Certain shikonin derivatives(such as Acetylshikonin) act as modulators of the Nur77-mediated apoptotic pathway and identify a new shikonin-based lead that targets Nur77 for apoptosis induction. 4. Acetylshikonin, shikonin, and alkannin have accelerative effect on the proliferation of granulation tissue in rats. 5. Acetylshikonin has inhibitory effect on the edematous response is due neither to the release of steroid hormones from the adrenal gland nor to the glucocorticoid activity, but probably partly to the suppression of mast cell degranulation and partly to protection of the vasculature from mediator challenge. 6. Acetylshikonin induces apoptosis of hepatitis B virus X protein-expressing human hepatocellular carcinoma cells via endoplasmic reticulum stress.

Monomethyl lithospermate (Lithospermic acid monomethyl ester) has potential antiviral activity, alleviating ischemic stroke injury in vivo in middle cerebral artery occlusion mice by activating PI5K/Akt signaling and protecting oxygen-glucose deprivation/reoxygenation-induced SHSY-3Y cells in vitro. Monomethyl lithospermate could improve the viability of SHSY-5Y cells, inhibit mitochondrial membrane potential (MMOP) collapse, and inhibit cell apoptosis. Monomethyl lithospermate also reduced the level of oxidative stress in the brain tissue of middle artery occlusion (MCAO) rats and improved nerve damage in ischemic stroke (IS) rats.

(2-Methylbutyryl)shikonin is a natural product from Lithospermum erythrorhizon Sieb. et Zucc.

(-)-5-Epilithospermoside is proposed as a potential marker of botanical origin for phacelia honey.

Shikonofuran A, a natural product, is isolated from Lithosperrrium erythrorhizon Sieb.

DL-Acetylshikonin can effectively inhibit tumor cells, it can be used to treat hepatocellular carcinoma cells expressing hepatitis B virus X protein (HBX) by inducing ER stress , an oncoprotein from hepatitis B virus. Acetylshikonin inhibits the production of eicosanoid, is due to the attenuation of cytosolic phospholipase A(2) membrane recruitment via the decrease in [Ca(2+)](i) and to the blockade of cyclooxygenase and 5-lipoxygenase activity.