R & D background

Professor Samuelsson and his team discovered leukotriene

Constructed a complete inflammatory basic theory of prostaglandins and leukotrienes, and won the Nobel Prize in medicine or physiology

Three kinds of drug discovery paths based on arachidonic acid and related inflammation basic theories:

Type I drug discovery pathway

Type I drug discovery pathway

Inhibiting the generation of inflammatory mediators: hormones, nonsteroidal anti-inflammatory drugs, zileuton and other drugs inhibit the inflammatory reaction by inhibiting phospholipase A2, cyclooxygenase / PGE isomerase (COX-1 and COX-2) and lipoxygenase, blocking the upstream pathway of arachidonic acid, inhibiting the production of prostaglandins and leukotrienes, the two major products of inflammation. While inhibiting inflammation, the above drugs inhibit the immune response to varying degrees. The use of these drugs is limited in the case of severe microbial infection, and they have different degrees of side effects.

The second type is drug discovery pathway

The second type is drug discovery pathway


Receptor antagonists of inflammatory mediators on cells: it is characterized in that it does not inhibit the production of prostaglandins and leukotrienes, but exerts anti-inflammatory and anti allergic effects through competitive binding with cellular receptors. It has no obvious inhibitory effect on the immune response - the target of such substances is clear, and drugs such as montelukast sodium have been successfully developed.

The third type is drug discovery pathway

The third type is drug discovery pathway


Substances produced by the human body in the process of fighting inflammation and injury, including small molecules and polypeptides, have strong activity and low effective concentration. They play a role through multiple targets and channels. The mechanism is complex and difficult to verify. After successful research and development, me too drugs are not easy to appear. Through the above drug development path, the team of etia has formed a number of small molecule compound candidate drugs and anti-inflammatory and anti fibrosis polypeptide compounds of multiple populations. Layout in the company's product line.

R & D pipeline

R & D pipeline


A new drug up818 for the treatment of acute lung injury and pulmonary fibrosis

Development process from acute lung inflammation to fibrosis


Action mechanism of up818

It can antagonize the receptor ligand interaction of tgfb1r2, CysLT1, DP2 (CRTH2), CXCR2 and other targets, and reduce the expression of CD14, TLR2 / 4 and IL-1R, as well as the expression of proinflammatory cytokines, so as to reduce the inflammatory response and damage of host cells to pathogen stimulation; Effectively down regulate the expression of heat shock proteins Hsp25, HSP60, HSP70, Hsp90 and other trauma related molecules, and reduce the expression and activation of inflammatory factors by downstream signaling pathways; It can also down regulate mitochondrial SOD enzyme and up regulate glutathione peroxidase, reduce the production of hydrogen peroxide and other superoxide ions, reduce the tissue damage caused by oxidative stress, down regulate CCL2, 3, 7, 12, 19 and CXCL1, 2, 3, 16, 17 and inhibit the chemotaxis of inflammatory cells; It can significantly regulate the expression of various leukocyte surface antigens and enhance the immune response of the host.

Strong data performance of up818 clinical study on upper respiratory tract antiviral


Cell line


IC50 (μM)

IC20 (μM)

CC50 (μM)



Vero E6


10.5 ± 1.96

2.63 ± 0.49

386.5 ±19



Vero E6

75% alcohol

8.74 ± 1.55

2.19 ± 0.39

386.5 ±19



Vero E6


10.11 ± 1.30

3.56 ± 0.46

386.5 ±19





9.51 ± 1.58

2.39 ± 0.39





75% alcohol

4.64 ± 0.66

3.69 ± 0.52





75% alcohol

5.19 ±0.33

3.57 ± 0.22

502.9 ± 209.7




75% alcohol

12.35 ± 1.39

6.00 ± 0.68




Vero E6

75% alcohol

5.32 ± 1.24

0.99 ± 0.23






0.38 ± 0.08




Montelukast sodium

Chronic wound formation originates from neuropathy and vascular disease

Neuropathy and vascular disease cause diabetes

Peripheral neuropathy leads to the weakening or disappearance of limb sensation, which reduces the feeling of pressure, foreign body or cold and heat in the foot, so it is easy to cause trauma and scald to form ulcers. Neuropathy is a possible cause of delayed wound healing in patients with diabetes. Vascular disease can lead to reduced blood flow of the lower limbs, hypoxia of the feet and insufficient nutrition supply, so the skin temperature of the lower limbs decreases, pain, intermittent claudication and ischemia, and in serious cases, ulcers and gangrene can be caused.

Neuropathy and vasculopathy lead to venous ulceration of lower limbs

At present, it is recognized that the pathogenesis is that the continuous venous hypertension of the lower extremities increases the transmural pressure of the blood vessels behind the capillaries, causing skin capillary damage, local blood circulation and tissue absorption disorder, chronic inflammatory reaction, metabolite accumulation, tissue malnutrition, lower extremity edema and skin nutrition changes, and finally leading to ulcer formation. Increased endothelial permeability and leukocyte infiltration, inflammatory cytokines, matrix metalloproteinases (MMP), reactive oxygen species and nitrogen species, iron deposition and tissue metabolites also contribute to the pathogenesis of vlu.

Effect of montelukast sodium:

Preclinical pharmacodynamic studies confirmed that montelukast sodium could reduce the nerve damage caused by oxidative stress and aging by up regulating the expression of tp53inp1, IDE and semaphorin. At present, clinical trials of 2 enterprises in the world are in progress, and the validation of montelukast sodium for mild to moderate Alzheimer's disease shows that montelukast sodium has the potential to improve neuropathy. The mechanism of peripheral neuropathy of chronic wound is similar to that of Alzheimer's disease, which will be observed as an exploratory end point in clinical trials.

Clinical study of montelukast sodium in treating chronic wounds of diabetes

Gene Symbol

Gene Bank Desc


Normal diabetes skin

Diabetes wound

High dose

Low dose


transformation related protein 53 inducible nuclear protein 1

It participates in the positive regulation of p53 transcriptional activity and mediates antioxidant related tumor suppressive function






insulin degrading enzyme

Degraded amyloid β Peptide - excess in Alzheimer's brain






sema domain, immunoglobulin domain (Ig), short basic domain, secreted, (semaphorin) 3C

Participate in nerve growth and guide axon orientation