Lifetein’s Photocleavable Linkers Assist Advancement of Microrobots in Anticancer Drug Delivery

The use of mobile microrobots offers a promising solution for targeted medical theranostic applications at normally inaccessible regions of the human body. Namely, the circulatory system is an ideal region for said applications, but blood flow can complicate both navigation inside the body and preservation of the microrobots.

Researchers have designed microrollers able to be controlled via magnetic propulsion and steering, able to maneuver against physiologically relevant blood flow effectively. The rollers are composed of a magnetically responsive half-side and a silica half-side for cargo loading and biochemical functionalities. Once navigated to cancerous cell monolayers, the rollers utilize surface-functionalized cell-specific antibodies as well as photocleavable linkers to release doxorubicin (DOX), and anticancer drug molecule, onto the target area.

Both the azide-DOX and o-nitrobenzyl photocleavable linker used by the team were provided by LifeTein, allowing the mircorollers to release the drug on demand via UV light exposure. This method of on demand delivery of the drug molecules combined with maneuverability of the microrollers designed by the researchers opens the door for development of next-generation microrobots for controlled navigation and cargo delivery in the circulatory system.

Reference: Alapan et al., Sci. Robot. 5, eaba5726 (2020) 20 May 2020


LifeTein’s Synthetic Scorpion Toxin Peptides Helped Nobel Prize Winner and Team Unravel Chronic Pain Mechanisms

Scorpion Toxin Peptides By Nobel Prize Winner David Julius

LifeTein’s synthetic Wasabi Receptor Toxin, Wasabi Receptor Toxin Mutants, Biotinylated Wasabi Receptor Toxin, and AlexaFluor-488 conjugated Wasabi Receptor Toxin and Mutants helped scientists unravel chronic pain mechanisms. Among this team was David Julius, corecipient of this year’s Nobel Prize in Physiology or Medicine.

Julius and fellow researchers at the University of California, San Francisco (UCSF) have identified a scorpion toxin that targets the “wasabi receptor”. The wasabi receptor is an ion channel protein that is responsible for the sinus-clearing or eye-stinging pain experienced when eating wasabi or chopping onions.

It was found that the scorpion toxin, a peptide as the wasabi receptor toxin, or WaTx, activates the wasabi receptor TRPA1 and triggers this pain response to irritants. The WaTx peptide is a novel cell-penetrating peptide and can directly pass through the plasma membrane, without needing to traverse through channel proteins.

The WaTx peptide could be used to study chronic pain and inflammation and may lead to the development of novel non-opioid pain therapies. WaTx produces pain and pain hypersensitivity, but not neurogenic inflammation.

Congratulations to David Julius, whose in-depth research in receptors lead to the discovery of receptors for temperature was rewarded with The Nobel Prize in Physiology or Medicine 2021.

Reference: Lin King, J. V., Emrick, J. J., Kelly, M. J. S., Herzig, V., King, G. F., Medzihradszky, K. F., & Julius, D. (2019). A Cell-Penetrating Scorpion Toxin Enables Mode-Specific Modulation of TRPA1 and Pain. Cell. doi:10.1016/j.cell.2019.07.014

Modified CPP Targets Essential Readers in H3K27M-DIPG

Histone H3K27M is a driving mutation in diffuse intrinsic pontine glioma (DIPG), a deadly pediatric brain tumor. The malignant and treatment-resistant brain tumor is a target for anti-cancer studies.


Through a global inhibition of PRC2 catalytic activity and displacement of H3K27me2/3, H3K27M reshapes the epigenome and promotes oncogenesis of DIPG. Consequentially, the histone modification H3K36me2, antagonistic to H3K27me2/3, is elevated. The relationship and role of H3K36me2 in H3K27M-DIPG was investigated by approaches to its upstream catalyzing enzymes, NSD1 and NSD2, the “writers”, and its downstream binding factors, LEDGF and HDGF2, the “readers”.


Tumor-promoting transcriptional programs in H3K27M-DIPG were found to be disrupted by loss of NSD1 and NSD2, thus impeding cellular proliferation and tumorigenesis.
Downstream, a chemically modified peptide mimicking endogenous H3K36me2 was found to dislodge LEDGF and HDGF2 from chromatin. As LEDGF and HDGF2 are the main readers mediating the protumorigenic effects downstream of NSD1/2-H3K36me2, dislodging them resulted in inhibition of H3K27M-DIPG proliferation.


In this study, the chemically modified peptides used were cell penetrating peptides purchased from LifeTein.

Reference: Sci. Adv. 2021 Jul 14; 7(29)