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romurtide (muroctasin / romurtide / Nopia)

✓ Approved

Daiichi Sankyo Company Limited · CSF1 · Small Molecule

What is romurtide?

romurtide is a small molecule developed by Daiichi Sankyo Company Limited. It is approved for therapeutic indications.

Drug Profile

Brand Namesmuroctasin, romurtide, Nopia
CompanyDaiichi Sankyo Company Limited
Drug ClassSmall Molecule, Polypeptide
Molecular TargetCSF1
StatusApproved
Sources: ClinicalTrials.gov, Daiichi Sankyo Company Limited

Mechanism of Action

Molecular Targets

romurtide acts on 1 molecular target:

CSF1colony stimulating factor 1 (MCSF, PG-M-CSF)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

romurtide is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Surgical and medical proceduresOral appliance application✓ Approved

Related Research Articles

PubMedJournal of immunology (Baltimore, Md. : 1950)2008-10-04

Differential effects of GM-CSF and G-CSF on infiltration of dendritic cells during early left ventricular remodeling after myocardial infarction.

Naito Kotaro K, Anzai Toshihisa T, Sugano Yasuo Y, Maekawa Yuichiro Y et al.

Several lines of evidence suggest that the immune activation after myocardial infarction (MI) induces secondary myocardial injury. Although dendritic cells (DC) are potent regulators of immunity, their role in MI is still undetermined. We investigated the effect of DC modulation by CSF on left ventricular (LV) remodeling after MI. MI was induced by ligation of the left coronary artery in male Wistar rats. G-CSF (20 microg/kg/day, MI-G, n = 33), a GM-CSF inducer (romurtide, 200 microg/kg/day, MI-GM, n = 28), or saline (MI-C, n = 55) was administered for 7 days. On day 14, MI-G animals had higher LV max dP/dt and smaller LV dimensions, whereas MI-GM animals had lower LV max dP/dt and larger LV dimensions than did MI-C animals, despite similar infarct size. In MI-C, OX62(+) DC infiltrated the infarcted and border areas, peaking on day 7. Bromodeoxyuridine-positive DC were observed in the border area during convalescence. Infiltration by DC was decreased in MI-G animals and increased in MI-GM animals compared with MI-C (p < 0.05). In the infarcted area, the heat shock protein 70, TLR2 and TLR4, and IFN-gamma expression were reduced in MI-G, but increased in MI-GM in comparison with those in MI-C animals. IL-10 expression was higher in MI-G and lower in MI-GM than in MI-C animals. In conclusion, G-CSF improves and GM-CSF exacerbates early postinfarction LV remodeling in association with modulation of DC infiltration. Suppression of DC-mediated immunity could be a new strategy for the treatment of LV remodeling after MI.

PMID 18832728
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PubMedNew biotechnology2008-09-13

Solid-state cultivation of Grifola frondosa (Dicks: Fr) S.F. Gray biomass and immunostimulatory effects of fungal intra- and extracellular beta-polysaccharides.

Svagelj Mirjan M, Berovic Marin M, Boh Bojana B, Menard Anja A et al.

Grifola frondosa strain GF3, was cultivated on solid-state substrate consisting of milled whole corn plant (Zea mays) and olive press cake supplemented with mineral additives and olive oil. Maintenance of the moisture content in the solid substrate is of crucial importance. Moistures higher than 70% promote growth of G. frondosa mycelium and polysaccharide production. Four fractions of pure extracellular beta-D-glucans with total mass 127.2mg and four fractions of intracellular polysaccharides with total mass 47.2mg were isolated. Polysaccharides were further separated by ion-exchange, gel and affinity chromatography. Isolated polysaccharide fractions from fungal mycelium proved to induce moderate amounts of TNF-alpha in PBMC cells in vitro. The extent of TNF-alpha induction was up to 322pgmL(-1) at a polysaccharide concentration of 200microgmL(-1) for the intracellular fraction. The TNF-alpha inducing activity is comparable to romurtide, which has been used as a supporting therapy in cancer patients treated with radiotherapy and/or chemotherapy.

PMID 18786661
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PubMedJournal of the American College of Cardiology2004-10-07

Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction.

Maekawa Yuichiro Y, Anzai Toshihisa T, Yoshikawa Tsutomu T, Sugano Yasuo Y et al.

We sought to determine the influence of granulocyte-macrophage colony-stimulating factor (GM-CSF) induction on post-myocardial infarction (MI) remodeling, especially in relation to the inflammatory response and myocardial fibrosis. Granulocyte-macrophage colony-stimulating factor modifies wound healing by promoting monocytopoiesis and infiltration of monocytes and macrophages into injured tissue; however, the effect of GM-CSF induction on the infarct healing process and myocardial fibrosis is unclear. A model of MI was produced in Wistar rats by ligation of the left coronary artery. The MI animals were randomized to receive GM-CSF inducer (romurtide 200 microg/kg/day for 7 consecutive days) (MI/Ro) or saline (MI/C). Echocardiographic and hemodynamic studies on day 14 revealed increased left ventricular (LV) end-diastolic dimension, decreased fractional shortening, elevated LV end-diastolic pressure, and decreased LV maximum rate of isovolumic pressure development in MI/Ro compared with MI/C. Immunoblotting showed that expression of transforming growth factor (TGF)-beta1 in the infarcted site on day 3 after MI was decreased in MI/Ro compared with MI/C. In the infarcted site, TGF-beta1, collagen type I and type III messenger ribonucleic acid (mRNA) expression on day 3, and collagen content on day 7 were reduced in MI/Ro compared with MI/C, in association with marked infarct expansion. In MI/Ro, monocyte chemoattractant protein-1 mRNA level and the degree of infiltration of monocyte-derived macrophages (ED-1-positive)were greater in the infarcted site on day 7 than those in MI/C. The GM-CSF induction by romurtide facilitated infarct expansion in association with the promotion of monocyte recruitment and inappropriate collagen synthesis in the infarcted region during the early phase of MI.

PMID 15464336
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PubMedJournal of biotechnology2003-05-29

Submerged cultivation of Ganoderma lucidum biomass and immunostimulatory effects of fungal polysaccharides.

Berovic Marin M, Habijanic Jozica J, Zore Irena I, Wraber Branka B et al.

Original Ganoderma lucidum strain MZKI G97 isolated from Slovenian forests was cultivated in a liquid substrate based on potato dextrose and olive oil. The influences of inoculum and oxygen partial pressure in batch and fed batch cultivation in a 10-l laboratory stirred tank reactor were studied. Fungal biomass was found to be oxygen and shear sensible. Using a 17% (wet weight) 6 days old vegetative inoculum, 9.6 g l(-1) of dry biomass in batch cultivation and 15.2 g l(-1) in fed batch process were obtained. Extracellular (9.6 g l(-1)) and intracellular (6.3 g l(-1)) polysaccharide fractions were isolated. Extracellular polysaccharide fraction and four intracellular polysaccharide fractions were obtained. Polysaccharides were further separated by ion-exchange, gel and affinity chromatography. The isolated polysaccharides were mainly beta-D-glucanes. Immunostimulatory effects of isolates were tested on induction of cytokine (tumour necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma)) synthesis in primary cultures of human peripheral blood mononuclear cells (PBMC) isolated from a buffy coat. The TNF-alpha inducing activity is comparable with romurtide, which has been used as a supporting therapy in cancer patients treated with radiotherapy and/or chemotherapy.

PMID 12770506
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PubMedInternational immunopharmacology2001-05-23

Induction of tumor necrosis factor-alpha in solid tumor region by the orally administered synthetic muramyl dipeptide analogue, romurtide.

Ueda H H, Yamazaki M M

The novel applications of a muramyl dipeptide analogue, romurtide, were investigated. When mice were intravenously injected with 10-1000 micrograms/mouse of romurtide as a primer and 3 KE/mouse of OK-432 as a trigger, systemic tumor necrosis factor-alpha (TNF-alpha) activity was increased. Similar effects were also detected by oral administration of romurtide at 1000 to 10,000 micrograms/mouse. These effects reached maximum at 3 h (intravenous injection, i.v.) or 6 h (oral administration, p.o.) after administration and were sustained for 48 h. When romurtide was administered to MM46 tumor-bearing mice orally, the significant augmentation of TNF-alpha production could be detected in the solid tumor and the liver. When romurtide was intravenously injected to the tumor bearer, the TNF-alpha production was significantly augmented in the spleen. These findings suggest that romurtide can augment the host defense system by both the parenteral and oral route, and indicate the possibility of a new type of anti-tumor therapy to induce TNF-alpha in the tumor region.

PMID 11367521
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PubMedPflugers Archiv : European journal of physiology2000-09-27

Modulation of tumour necrosis factor production with desmuramyldipeptide analogues.

Simcic S S, Wraber B B, Sollner M M, Urleb U U et al.

Some synthetic analogues of the immunomodulatory agent muramyl dipeptide (MDP), i.e. phthalimido- (LK-511, LK-413, LK-512, LK-423, LK-508), adamantyl- (LK-415, LK-517), 7-oxoalkyl-(LK-409) desmuramylpeptides were assessed for the tumour necrosis factor (TNF) inducing activity and the ability to modulate TNF production in in vitro phorbol 12-myristate 13-acetate (PMA) & ionomycin stimulated cultures of human peripheral blood mononuclear cells. A kinetic study over a 40-hour period indicated that desmuramyldipeptides were weak TNF inducers compared to romurtide, PMA & ionomycin or lipopolysaccharide. By contrast, they showed the potential to up- or down-regulate the production of TNF evoked by PMA & ionomycin, which was strongly dependent on the time of the stimulation. After 4h of stimulation, the TNF secretion was augmented by LK-508, LK-409 and LK-511, after 18 h by LK-409 and LK-423, and after 40 h by LK-423, LK-511, LK-415 and LK-512. However, LK-517 and LK-512 inhibited the secretion of TNF after the 18-h period.

PMID 11005615
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