The Info List - Belimumab

--- Advertisement ---

(trade name Benlysta, previously known as LymphoStat-B) is a human monoclonal antibody that inhibits B-cell activating factor (BAFF),[1] also known as B-lymphocyte stimulator (BLyS).[2] B cells are responsible for part of the normal immune response, and also for the over-aggressive immune response in autoimmune diseases like systemic lupus erythematosus (SLE). Belimumab
is approved in the United States, Canada
and Europe for treatment of SLE. However, the major phase III trials excluded the more severe cases of SLE with kidney and brain damage, so its effectiveness has not been demonstrated in those cases. A Phase III study for SLE patients with kidney disease is now recruiting.[3] U.S. F.D.A. reviewers were concerned that belimumab is only "marginally" effective, and that there were more deaths in the treatment group. Belimumab's defenders said that in addition to its modest efficiency, belimumab allowed patients to significantly reduce their use of corticosteroids.[4] Belimumab
is expensive, typically $28,000 for the first year. The UK National Institute for Health and Care Excellence (NICE) calculated the cost of belimumab at £61,200 per quality-adjusted life year (QALY), which is more than the normally accepted £20,000 to £30,000. Phase II trials of belimumab for rheumatoid arthritis were unsuccessful. Phase II trials for Sjögren’s Syndrome were more successful. Belimumab
was developed by Human
Genome Sciences (HGS) and Cambridge Antibody
Technology.[5] GlaxoSmithKline
acquired HGS, took belimumab through Phase III clinical trials, and markets belimumab.[6]


1 Uses

1.1 Systemic lupus erythematosus 1.2 Rheumatoid arthritis 1.3 Sjögren’s Syndrome

2 Side effects 3 Interactions 4 Mechanism of action 5 Discovery and history 6 FDA approval 7 Costs 8 Other drugs addressing B lymphocyte
B lymphocyte
hyperactivity 9 References

Uses[edit] Systemic lupus erythematosus[edit] While belimumab appears safe in systemic lupus erythematosus, the magnitude of benefit is small.[7] Black patients did not show a benefit. The most severe cases, with kidney and central nervous system involvement, were excluded from the trials. The efficacy and safety of belimumab was demonstrated in 2 Phase III randomized, controlled studies, BLISS-52[8] and BLISS-76.[9] The 2 studies had a total of 1,684 patients, with scores of ≥6 on the SELENA-SLEDAI assessment. They were divided into a placebo and 2 dosage groups of belimumab, in addition to standard therapy. The primary end point was a reduction of ≥4 on the SELENA-SLEDAI assessment, and several other factors, at 52 weeks. Belimumab significantly improved the response rate, reduced disease activity and severe flares, and was well tolerated. 58% had SELENA-SLEDAI scores reduced by ≥4 points during 52 weeks with belimumab 10 mg/kg compared to 46% with placebo. Benlysta was the first new drug to treat lupus after 56 years. Sales rose to $31.2 million in the first quarter of 2012.[10] It is marketed by GlaxoSmithKline
and sold for about US$35,000 per year per patient. Rheumatoid arthritis[edit] In phase II clinical trials for rheumatoid arthritis.[11] belimumab was not effective.[7] Sjögren’s Syndrome[edit] Belimumab
has completed phase II trials for Sjögren’s Syndrome.[12] Side effects[edit] Common adverse effects reported with belimumab include nausea, diarrhea, fever, as well as hypersensitivity and infusion-site reactions (severe in 0.9% of patients). It is suggested that patients be treated with an antihistamine prior to a belimumab infusion.[13] A greater number of serious infections and deaths were reported in patients treated with belimumab than in those treated with placebo. Infections are due to the immunosuppressant properties of the drug.[14] Interactions[edit] No interaction studies have been carried out. Combination of belimumab with other immunosuppressants, especially those targeting B lymphocytes such as anti- CD20
therapies, could increase the risk of severe infections. Likewise, the combination with intravenous cyclophosphamide is not recommended, as well as administering live vaccines during treatment with belimumab.[13][15] Mechanism of action[edit] B lymphocytes (B cells) are one of the immune cells responsible for the damage in autoimmune disease. B cells develop in the bone marrow and continue to mature peripherally in secondary lymphoid organs and (as recently discovered) in the gut. When autoimmune B cells attack the body's own tissues, they are normally destroyed by cell suicide (apoptosis). In order to survive, B cells need survival factors. Researchers theorize that SLE is caused when autoimmune B cells proliferate, and survival factors protect them from cell suicide. B-cell activating factor
B-cell activating factor
(BAFF), also called B-lymphocyte stimulator (BLyS), is required for the development and survival of B cells. In SLE, BAFF is overexpressed. Researchers theorize that BAFF overexpression causes autoimmune B cell proliferation and survival, which causes SLE. Belimumab
is a human antibody that binds to BAFF, preventing BAFF from binding to B cells. Without the survival factor BAFF, B cells commit suicide, and no longer contribute to the autoimmune damage of SLE. BAFF is secreted by a variety of cells: monocytes and macrophages, bone marrow stromal cells, astrocytes, synoviocytes during rheumatoid arthritis, salivary epithelial cells during Sjögren's syndrome, astrocytes in certain glioblastomas. BAFF interacts with three membrane receptors on B lymphocytes:

(BAFF receptor) BCMA (B cell maturation antigen) TACI
(transmembrane activator and calcium modulator and cyclophylin ligand interactor)

When BAFF binds to BAFF-R
and BCMA on B cells, levels of Bcl-2, a survival factor, are increased. When all three BAFF receptors are stimulated, levels of NF kappa B, which contributes to cell proliferation and differentiation, are increased in the nucleus. Another B-cell activator like BAFF is APRIL (a proliferation-inducing ligand),[16] but APRIL only activates BCMA and TACI, not BAFF-R. Belimumab
reduces the number of circulating B cells, but anti-CD20 monoclonal antibodies reduce the number even more. It is possible that belimumab binds primarily to circulating soluble BAFF, therefore not inducing antibody-dependent cellular cytotoxicity that could be expected from this IgG1-type antibody.[17][Better, more current citation needed] Discovery and history[edit] B-cell activating factor
B-cell activating factor
is a naturally occurring protein that was discovered by researchers from National Jewish Health
National Jewish Health
(previously the National Jewish Medical and Research Center) and the University of Colorado, who collaboratively published a paper detailing their findings in May 1999, naming the protein TALL-1.[18] The same protein was named BAFF in another paper published in June 1999; and in a paper published in July of that year, Human
Genome Sciences (HGS) referred to it as BLyS (or B lymphocyte
B lymphocyte
stimulator).[19] Six years later, the key role of BLyS in B cell differentiation, survival and activation was published.[20] Five years prior, in October 2000, HGS and Cambridge Antibody Technology (CAT) agreed to co-develop monoclonal antibodies targeted at BLyS. Under this agreement, CAT would identify antibodies and HGS would select appropriate ones to take into clinical trials.[21] In 2003, CAT researchers reported that, by using phage display technology, they had elicited an array of over 1000 distinct antibodies, half of which inhibited binding of BLyS to its receptor.[5] Later that year, one of these antibodies was isolated and characterized. It was named LymphoStat-B and subsequently called belimumab.[22] In August 2006, HGS and GlaxoSmithKline
(GSK) entered into a co-development and commercialization agreement under which HGS would conduct Phase 3 trials for belimumab with assistance from GSK. The companies would share equally in Phase 3/4 development costs, sales and marketing expenses, and profits of any product commercialized under the agreement.[21] On February 13, 2007, HGS and GSK announced the initiation of the first of two pivotal Phase 3 clinical trial of belimumab in patients with active lupus erythematosus.[6] FDA approval[edit] Under its trade name Benlysta, belimumab was approved by the U.S. Food and Drug Administration (FDA) for treatment of SLE on March 9, 2011.[23] The FDA Advisory committee approved it with a 13-to-2 vote, despite reservations that the improvement of only 4 points on the SELENA-SLEDA scale was only marginally effective, and despite reservations about additional deaths in the treatment group.[24][25] Based on the number needed to treat, approximately eleven patients must be treated for one to benefit. It was not tested in severe forms of SLE, which involve active damage to the kidneys or central nervous system in the phase III trials. Subjects with active kidney disease were included in the Phase II trials of the drug.[26] "Patients with active lupus that involved the kidneys ... were excluded from participating in the trials. Study participants of African American or African descent did not significantly respond to belimumab."[24][27][28] It has subsequently been approved for use in Europe and Canada.[29] Costs[edit] Belimumab
is expensive. At a typical U.S. academic center, the total cost for the first year of treatment is $28,000. Annual prices of generic prescription drugs are prednisone, $140; hydroxychloroquine, $132; oral methotrexate, $432; azathioprine, $468; and mycophenolate mofetil, $1,224.[30] In the UK, the National Institute for Health and Care Excellence (NICE) calculated the cost of belimumab at £61,200 per quality adjusted life year (QALY). This is more than the normally accepted cost of £20,000 to £30,000 per QALY. The manufacturer offered the UK National Health Service a discount, the amount of which were confidential, which still did not bring it into the acceptable range.[31] Other drugs addressing B lymphocyte
B lymphocyte
hyperactivity[edit] Atacicept
is a recombinant fusion protein built with the extracellular ligand binding portion of TACI. It blocks activation of TACI
by APRIL and BLyS. It failed a phase II trial for multiple sclerosis.[32] Blisibimod, an inhibitor of both soluble and membrane bound BAFF, has demonstrated similar reductions of B cells in clinical trials and is being investigated in a phase 2 clinical study for patients with lupus erythematosus. BR3-Fc is a recombinant fusion protein built with the extracellular ligand-binding portion of BAFF-R. It blocks activation of this receptor by BLyS, and is in early stage pharmaceutical development.[33] Of anti- CD20
monoclonal antibodies, rituximab has been approved for some indications. Ocrelizumab, ofatumumab and "third generation" anti- CD20
monoclonals are in development. References[edit]

^ Bossen, C; Schneider, P (October 2006). "BAFF, APRIL and their receptors: structure, function and signaling". Semin. Immunol. 18 (5): 263–75. doi:10.1016/j.smim.2006.04.006. PMID 16914324.  ^ Srini V. Kaveri; Luc Mouthon & Jagadeesh Bayry (September 9, 2010). "Clinical Implications of Basic Research: Basophils and Nephritis in Lupus". N Engl J Med. 363 (11): 1080–1082. doi:10.1056/NEJMcibr1006936. PMID 20825323.  ^ Efficacy and Safety of Belimumab
in Patients With Active Lupus Nephritis (BLISS-LN), NCT01639339 ^ Should Belimumab
Have Been Approved? Stephen Paget, Medscape Rheumatology, Mar 24, 2011 ^ a b Edwards BM, Barash SC, Main SH, et al. (November 2003). "The remarkable flexibility of the human antibody repertoire; isolation of over one thousand different antibodies to a single protein, BLyS". J. Mol. Biol. 334 (1): 103–18. doi:10.1016/j.jmb.2003.09.054. PMID 14596803.  ^ a b " Human
Genome Sciences And Glaxosmithkline Announce Initiation Of Phase 3 Clinical Trial Of Lymphostat-B In Systemic Lupus Erythematosus" (Press release). Human
Genome Sciences. 2007-02-13. Archived from the original on 25 April 2011. Retrieved 2011-03-11.  ^ a b Belimumab: The 1st drug to be FDA approved for the treatment of lupus since 1955, By Rebecca Manno, Johns Hopkins Arthritis Center, July 15, 2011 ^ Navarra SV; Guzmán RM; Gallacher; BLISS- Study Group; et al. (Feb 26, 2011). "Efficacy and safety of belimumab in patients with active systemic lupus erythematosus: a randomised, placebo-controlled, phase 3 trial". Lancet. 377 (9767): 721–31. doi:10.1016/S0140-6736(10)61354-2. PMID 21296403.  ^ Furie R; Petri M; Zamani O; BLISS- Study Group; et al. (December 2011). "A phase III, randomized, placebo-controlled study of belimumab, a monoclonal antibody that inhibits B lymphocyte stimulator, in patients with systemic lupus erythematosus". Arthritis Rheum. 63 (12): 3918–30. doi:10.1002/art.30613. PMID 22127708.  ^ HGSI Cuts Loss on Benlysta Sales, By Zacks Equity Research, Apr 26, 2012 ^ Clinical trial
Clinical trial
number NCT00071812 for "A Safety and Efficacy Study of LymphoStat-B (Monoclonal Anti-BLyS Antibody) in Subjects With Rheumatoid Arthritis" at ClinicalTrials.gov, ^ Efficacy and Safety of Belimumab
in Subjects With Primary Sjögren's Syndrome (BELISS) ^ a b European Medicines Agency: Benlysta Summary of Product Characteristics ^ " GlaxoSmithKline
and Human
Genome Sciences announce FDA approval of Benlysta (belimumab) for the treatment of systemic lupus erythematosus". GlaxoSmithKline. 9 March 2011. Archived from the original on March 17, 2011. Retrieved 11 March 2011.  ^ Drugs.com: Benlysta Official FDA information, side effects and uses ^ Schneider P (2005). "The role of APRIL and BAFF in lymphocyte activation". Curr. Opin. Immunol. 17 (3): 282–9. doi:10.1016/j.coi.2005.04.005. PMID 15886118.  ^ June 2007 European League against Rheumatism symposium. ^ Shu HB, Hu WH, Johnson H (May 1999). "TALL-1 is a novel member of the TNF family that is down-regulated by mitogens". J. Leukoc. Biol. 65 (5): 680–3. PMID 10331498.  ^ Moore, PA; Belvedere, O; Orr, A; Pieri, K; Lafleur, DW; Feng, P; Soppet, D; Charters, M; Gentz, R; Parmelee, D; Li, Y; Galperina, O; Giri, J; Roschke, V; Nardelli, B; Carrell, J; Sosnovtseva, S; Greenfield, W; Ruben, SM; Olsen, HS; Fikes, J; Hilbert, DM (July 1999). "BLyS: member of the tumor necrosis factor family and B lymphocyte stimulator". Science. 285 (5425): 260–3. doi:10.1126/science.285.5425.260. PMID 10398604.  ^ Crowley JE, Treml LS, Stadanlick JE, Carpenter E, Cancro MP (2005). "Homeostatic niche specification among naïve and activated B cells: a growing role for the BLyS family of receptors and ligands". Semin. Immunol. 17 (3): 193–9. doi:10.1016/j.smim.2005.02.001. PMID 15826824.  ^ a b "Benlysta (belimumab)". Human
Genome Sciences. Archived from the original on 21 April 2011. Retrieved 2011-03-11.  ^ Baker KP, Edwards BM, Main SH, et al. (November 2003). "Generation and characterization of LymphoStat-B, a human monoclonal antibody that antagonizes the bioactivities of B lymphocyte
B lymphocyte
stimulator". Arthritis Rheum. 48 (11): 3253–65. doi:10.1002/art.11299. PMID 14613291.  ^ "FDA approves Benlysta to treat lupus" (Press release). U.S. Food and Drug Administration (FDA). March 9, 2011.  ^ a b FDA Questions Safety, Efficacy of Belimumab, By Emily P. Walker, Washington Correspondent, MedPage Today, November 12, 2010 ^ F.D.A. Panel Backs Drug for Lupus By ANDREW POLLACK, New York Times, November 16, 2010M ^ Andrew Pollack, "F.D.A. Approves Benlysta, a New Lupus Drug", The New York Times, March 9, 2011 ^ Summary Minutes of the Arthritis Advisory Committee Meeting November 16, 2010 U.S. Food and Drug Administration
U.S. Food and Drug Administration
(FDA) ^ 2010 Meeting Materials, Arthritis Advisory Committee U.S. Food and Drug Administration (FDA) ^ WRAL Tech Wire: GSK wins OK for Lupus drug in Europe, Canada ^ Bevra Hannahs Hahn (April 18, 2013). " Belimumab
for Systemic Lupus Erythematosus". N Engl J Med. 368 (16): 1528–1535. doi:10.1056/NEJMct1207259. PMID 23594005.  ^ NICE publishes draft guidance on belimumab for systemic lupus erythematosus, press release, 26 April 2012 ^ Clinical trial
Clinical trial
number NCT00642902 for " Atacicept
in Multiple Sclerosis, Phase II" at ClinicalTrials.gov ^ Vugmeyster, Y.; Seshasayee, D.; Chang, W.; Storn, A.; Howell, K.; Sa, S.; Nelson, T.; Martin, F.; Grewal, I.; Gilkerson, E.; Wu, B.; Thompson, J.; Ehrenfels, B. N.; Ren, S.; Song, A.; Gelzleichter, T. R.; Danilenko, D. M. (2006). "A Soluble BAFF Antagonist, BR3-Fc, Decreases Peripheral Blood B Cells and Lymphoid Tissue Marginal Zone and Follicular B Cells in Cynomolgus Monkeys". The American Journal of Pathology. 168 (2): 476–489. doi:10.2353/ajpath.2006.050600. PMC 1606502 . PMID 16436662. 

v t e

Immunosuppressive drugs / Immunosuppressants

Intracellular (initiation)


purine synthesis inhibitors

Azathioprine Mycophenolic acid

pyrimidine synthesis inhibitors

Leflunomide Teriflunomide



Macrolides/ other IL-2 inhibitors


Tacrolimus Ciclosporin Pimecrolimus

Abetimus Gusperimus


Lenalidomide Pomalidomide Thalidomide PDE4 inhibitor


Intracellular (reception)

IL-1 receptor antagonists



Sirolimus Everolimus Ridaforolimus Temsirolimus Umirolimus Zotarolimus




Serum target (noncellular)

Complement component 5



Adalimumab Afelimomab Certolizumab pegol Golimumab Infliximab Nerelimomab



Immunoglobulin E






IL-12 and IL-23

Lebrikizumab Ustekinumab



Cellular target


Muromonab-CD3 Otelixizumab Teplizumab Visilizumab


Clenoliximab Keliximab Zanolimumab






Obinutuzumab Rituximab Ocrelizumab Pascolizumab


Gomiliximab Lumiliximab


Teneliximab Toralizumab










Belimumab Blisibimod


Ipilimumab Tremelimumab


Bertilimumab Lerdelimumab Metelimumab



Interleukin-6 receptor




IL-2 receptor/CD25

Basiliximab Daclizumab Inolimomab

T-lymphocyte (Zolimomab aritox)


Atorolimumab Cedelizumab Fontolizumab Maslimomab Morolimumab Pexelizumab Reslizumab Rovelizumab Siplizumab Talizumab Telimomab aritox Vapaliximab Vepalimomab


Anti-thymocyte globulin Anti-lymphocyte globulin

-cept (Fusion)


Abatacept Belatacept

TNF inhibitor

Etanercept Pegsunercept

Aflibercept Alefacept Rilonacept

v t e

Monoclonal antibodies
Monoclonal antibodies
for the immune system

Immune system
Immune system


Immunosuppression: Abrilumab Adalimumab Anifrolumab† Atorolimumab Avelumab Belimumab Bleselumab Brodalumab Camidanlumab tesirine Carlumab Cemiplimab Dupilumab Eldelumab Emapalumab† Fresolimumab Gimsilumab Golimumab Lanadelumab Lenzilumab Lerdelimumab Lirilumab Mavrilimumab Metelimumab Morolimumab Namilumab Oleclumab Oxelumab§ Pamrevlumab Placulumab Sarilumab Sifalimumab Tabalumab Tezepelumab† Ulocuplumab Varlilumab

Immune activation: Ipilimumab Atezolizumab Durvalumab Nivolumab Pembrolizumab Tremelimumab† Urelumab

Other: Bertilimumab Zanolimumab

Mouse ("-limo-")

Afelimomab Elsilimomab Faralimomab Gavilimomab Inolimomab Maslimomab Nerelimomab Odulimomab Telimomab aritox Vepalimomab Zolimomab aritox

Chimeric ("-lixi-")

Andecaliximab† Basiliximab Clenoliximab Galiximab Gomiliximab Infliximab Keliximab Lumiliximab Priliximab Teneliximab Vapaliximab

Humanized ("-lizu-")

Immunosuppressive: Aselizumab Apolizumab§ Benralizumab Cedelizumab Certolizumab pegol Crizanlizumab† Daclizumab Eculizumab Efalizumab Epratuzumab Erlizumab Etrolizumab† Fontolizumab Inebilizumab† Itolizumab Lampalizumab† Letolizumab Ligelizumab Lulizumab pegol Mepolizumab Mogamulizumab Natalizumab Ocrelizumab Omalizumab Ozoralizumab Pascolizumab Pateclizumab Pembrolizumab Pexelizumab Pidilizumab Plozalizumab PRO 140† Quilizumab Ravulizumab† Reslizumab Rontalizumab Rovelizumab Ruplizumab Samalizumab Siplizumab Talizumab Teplizumab Tibulizumab Tislelizumab Tocilizumab Toralizumab Tregalizumab Vatelizumab Vedolizumab Visilizumab Vobarilizumab TGN1412§ Non-immunosuppressive: Ibalizumab

Chimeric + humanized ("-lixizu-")

Otelixizumab Tavolimab

Veterinary ("-lvet-")




Brazikumab Briakinumab Canakinumab Fezakinumab Fletikumab Guselkumab Secukinumab Sirukumab Tralokinumab† Ustekinumab

Humanized ("-kizu-", "-kinzu-")

Anrukinzumab Clazakizumab Enokizumab Gevokizumab Ixekizumab Mirikizumab Lebrikizumab Olokizumab† Perakizumab Risankizumab† Tildrakizumab

Inflammatory lesions ("-les-")

Mouse ("-leso-")

Besilesomab Fanolesomab‡ Lemalesomab Sulesomab

#WHO-EM ‡Withdrawn from market Clinical trials:

†Phase III §Never to phase III

v t e

Cytokine receptor
Cytokine receptor


See here instead.



Agonists: ARA-290 Asialo erythropoietin Carbamylated erythropoietin CNTO-530 Darbepoetin alfa Epoetin alfa Epoetin beta Epoetin delta Epoetin epsilon Epoetin gamma Epoetin kappa Epoetin omega Epoetin theta Epoetin zeta Erythropoietin
(EPO) Erythropoietin-Fc Methoxy polyethylene glycol-epoetin beta
Methoxy polyethylene glycol-epoetin beta
(CERA/Mircera) Peginesatide Pegol sihematide (EPO-018B)


Agonists: Filgrastim Granulocyte colony-stimulating factor Lenograstim Leridistim Lipegfilgrastim Nartograstim Pegfilgrastim Pegnartograstim


Agonists: Ecogramostim Granulocyte macrophage colony-stimulating factor Milodistim Molgramostim Regramostim Sargramostim

Antibodies: Mavrilimumab MOR103 Namilumab


Agonists: Cilmostim Interleukin-34 Lanimostim Macrophage
colony-stimulating factor Mirimostim

Kinase inhibitors: Agerafenib

SCF (c-Kit)

See here instead.


Agonists: Eltrombopag Pegacaristim Promegapoietin Romiplostim Thrombopoietin


IFNAR (α/β, I)

Agonists: Albinterferon Interferon
alpha (interferon alfa, IFN-α) Interferon
alfa (IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16, IFNA17, IFNA21) Interferon
alfa 2a Interferon
alfa 2b Interferon
alfa n1 Interferon
alfacon-1 Interferon
alpha-n3 Interferon
beta (IFN-β) (IFNB1, IFNB3) Interferon
beta 1a Interferon
beta 1b Interferon
kappa (IFN-ε/κ/τ/ζ, IFNK) Interferon
omega (IFN-ω, IFNW1) Peginterferon alfa-2a Peginterferon alfa-2b

Antibodies: Anifrolumab Faralimomab MEDI-545 Rontalizumab Sifalimumab

Decoy receptors: Bifarcept


Agonists: Interferon
gamma (IFN-γ) Interferon
gamma 1b

Antibodies: Emapalumab Fontolizumab


See IL-28R (IFNLR) here instead.


See here instead.


See here instead.


See here instead.


JAK (inhibitors)


Baricitinib Filgotinib Momelotinib Oclacitinib Ruxolitinib Tofacitinib
(tasocitinib, CP-690550) Upadacitinib


AG-490 Atiprimod AZD-1480 Baricitinib CHZ868 Cucurbitacin I
Cucurbitacin I
(elatericin B, JSI-124) CYT387 Lestaurtinib NSC-7908 NSC-33994 Pacritinib Ruxolitinib SD-1008 Tofacitinib
(tasocitinib, CP-690550)


AG-490 Cercosporamide TCS-21311 Tofacitinib
(tasocitinib, CP-690550) WHI-P 154 ZM-39923 ZM-449829


Additional cytokines: Cardiotrophin 1 (CT-1) FMS-like tyrosine kinase 3 ligand (FLT3L) Leukemia/leukocyte inhibitory factor (LIF) Oncostatin M
Oncostatin M
(OSM) Thymic stromal lymphopoietin
Thymic stromal lymphopoietin

Additional cytokine receptor modulators: Emfilermin Lestaurtinib Midostaurin Quizartinib Sorafenib Sunitinib

See also Receptor/signaling modulators Signaling peptide/protein receptor modulators Growth factor r