







































 

_____________________________________________________________________________________________________ 
 
++ Assistant Professor; 
# Pharm D III Year; 
*Corresponding author: E-mail: keshapallysrijareddy@gmail.com; 
 
Cite as: Gupta, Nikita, Sai Rama Konda, K. Srija, and G. Pooja Reddy. 2024. “The Mechanism and Efficacy of Baricitinib As a 
Novel Therapeutic Option for Rheumatoid Arthritis: A Review”. Asian Journal of Immunology 7 (1):123-30. 
https://journalaji.com/index.php/AJI/article/view/137. 
 

 
 

Asian Journal of Immunology 
 
Volume 7, Issue 1, Page 123-130, 2024; Article no.AJI.120135 
 

 
 

 

 

The Mechanism and Efficacy of 
Baricitinib as a Novel Therapeutic 
option for Rheumatoid Arthritis: A 

Review 
 

Nikita Gupta a++, Sai Rama Konda b#, K. Srija b#*  
and G. Pooja Reddy b# 

 
a Department of Pharmacy Practice, St. Pauls College of Pharmacy, Turkayamjal, Hyderabad, 

Telangana, India. 
b St. Pauls College of Pharmacy, Turkayamjal, Hyderabad, Telangana, India. 

 

Authors’ contributions  
 

This work was carried out in collaboration among all authors. All authors read and approved the final 
manuscript. 

 

Article Information 
 

DOI: https://doi.org/10.9734/aji/2024/v7i1137  
 

Open Peer Review History: 
This journal follows the Advanced Open Peer Review policy. Identity of the Reviewers, Editor(s) and additional Reviewers,  

peer review comments, different versions of the manuscript, comments of the editors, etc are available here: 
https://www.sdiarticle5.com/review-history/120135  

 
 

Received: 03/06/2024 
Accepted: 05/08/2024 
Published: 23/08/2024 

 
 

ABSTRACT 
 

Rheumatoid arthritis (RA) is characterized by systemic synovitis, which destroys joints. With the 
discovery of biological disease-modifying anti-rheumatic medicines (bDMARDs) and the 
combination of traditional DMARDs, clinical remission is now seen as a reasonable and achievable 
aim for many patients. However, bDMARDs must be administered via intravenous or subcutaneous 
injection, and some patients may not react or lose their main response. Under these conditions, 
targeted synthetic DMARDs (tsDMARDs), which are low.  

Review Article 

https://doi.org/10.9734/aji/2024/v7i1137
https://www.sdiarticle5.com/review-history/120135


 
 
 
 

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124 

 

molecular-weight molecules that may be taken orally, have emerged. Five phase 3 studies of 
Baricitinib, a JAK1(janus kinase1) and JAK2(janus kinase 2) inhibitor, demonstrated good clinical 
effectiveness in patients with active RA who were naïve to sDMARDs or had an unsatisfactory 
response to sDMARDs, MTX(methotrexate) or bDMARDs. In patients with rheumatoid arthritis who 
had not previously been treated with biologic disease-modifying Antirheumatic medications 
(DMARDs), Baricitinib, an oral inhibitor of Janus kinase 1 and 2, decreased disease activity. 

 

 
Keywords: Rheumatoid arthritis; Baericitinib; bDMARDS; tsDMARDs; JAK1 inhibitor; JAK2 inhibitors; 

MTX. 
 

1. INTRODUCTION 
 
“Rheumatoid arthritis (RA) is a systemic 
autoimmune illness linked to a persistent 
inflammatory process that can harm extra-
articular organs such as the kidney, lung, heart, 
digestive tract, eyes, skin, and nervous system in 
addition to joints. To categorise arthritis into non-
inflammatory (osteoarthritis) and inflammatory 
(pseudogout, basic calcium phosphate disease, 
gout) types, as well as bacterial and viral 
infections (Staphylococcus aureus, Neisseria 
gonorrhoeae, complications of Lyme disease, 
parvovirus, enterovirus), and autoimmune 
processes, a great deal of research and 
description has been done on arthritis” [1].  
 
“Systemic synovitis-induced joint degradation is 
a characteristic feature of rheumatoid arthritis 
(RA)” [1]. “When chondrocytes and fibroblasts 
are stimulated, cartilage and bone are broken 
down, leading to the production of osteoclasts 
and metalloproteinases and joint injury” [2,3]. 
“These processes are facilitated by the 
overproduction of pro-inflammatory cytokines by 
immune cells in the synovium, such as 
macrophage colony stimulating factor, 
interleukins-6 and-17, and tumor necrosis factor-
α” [2,4]. “This medication has been authorized by 
the FDA for use in adult patients with moderately 
to severely active rheumatoid arthritis when other 
DMARDs, such as tumor necrosis factor 
antagonist therapies, have not proven to be 
helpful” [5]. “Baricitinib is an oral selective 
inhibitor of JAK1 and JAK2, specifically 
formulated to treat patients with active 
rheumatoid arthritis” [6].  
 
“Baricitinib, a JAK1 and JAK2 inhibitor, has been 
subjected to five phase 3 trials that have 
demonstrated excellent clinical efficacy in 
patients with active RA who have not responded 
well to sDMARDs, MTX, or bDMARDs. 
Adalimumab, MTX, and placebo were used as 
comparators in studies where there was a 
positive response for clinical and functional 

criteria. Additionally, it is stated that safety was 
bearable within the short trial duration” [1,7,8].  
 
“JAK inhibitors provide an alternative to 
traditional RA treatments by targeting cytokine 
signaling pathways linked to the pathophysiology 
of RA. In clinical studies including individuals 
with RA 1–5, the oral, selective JAK1 and JAK2 
inhibitor baricitinib has demonstrated clinical 
effectiveness and tolerability. Adults with 
moderately-to severely active RA are eligible to 
receive baricitinib therapy in over 50 countries, 
including the US, Japan, and several European 
nations” [9].  
 
The main therapy goal for individuals with 
established RA is to achieve minimal disease 
activity [10,11] . “Many DMARD treatments have 
been tried by a sizable portion of patients with 
established RA, but they have not been 
successful in reaching a low disease activity 
state. According to clinical research, response 
rates to all presently prescribed medications 
decline as cDMARD and bDMARD experience 
increases” [12]. “Studies involving patients who 
have not responded to prior bDMARDs are 
especially significant since this cohort is growing 
and has the biggest unmet demand in the RA 
field. The RA-BEACON trial did not previously 
evaluate the degree to which patient variables, 
such as age, illness duration, serological status, 
or history of using certain bDMARDs, impact the 
response to baricitinib” [13]. These crucial 
queries are covered in the present                     
analysis [14]. 
 
“This article aims to compile and summarize the 
available information about the impact of 
baricitinib on the development of structural joint 
damage as well as the underlying mechanisms 
of these effects. Results measured by magnetic 
resonance imaging (MRI) or radiographic 
progression of joint erosion and joint space 
narrowing in clinical studies and post analyses of 
patients with RA who are naive to disease-
modifying antirheumatic drugs (DMARDs) or who 



 
 
 
 

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do not respond well to conventional synthetic 
DMARDs (csDMARDs) are presented. These 
results were obtained with approved doses of 
baricitinib (2 mg or 4 mg once daily, except in the 
USA, Canada, and China, where the approved 
dose is 2 mg once daily). Furthermore, 
preclinical baricitinib study results are discussed” 
[2].  
 
“When traditional DMARDs are insufficient for 
treating rheumatoid arthritis, baricitinib, a 
disease-modifying anti-rheumatic medication, 
may be used. Adult patients with                        
moderately to severely active rheumatoid arthritis 
who have not reacted well to previous DMARDs, 
including tumor necrosis factor antagonist 
treatments, may use this medicine, according to 
approval from the U.S. Food and Drug 
Administration (FDA). Moreover, baricitinib is 
FDA approved for the treatment of COVID-19, 
making it a viable option for hospitalized patients 
when combined with other medications. This 
includes pediatric instances that require 
extracorporeal membrane oxygenation, invasive 
mechanical ventilation, or supplemental oxygen. 
Reviewing all the important information on 
baricitinib therapy in the clinical setting, including 
mechanisms, side effects, and contraindications, 
is the aim of this exercise. This exercise is 
specifically designed to fulfill the requirements of 
an interdisciplinary medical team that treats 
patients with rheumatoid arthritis, alopecia 
areata, and COVID -19” [5] concluded by et al 
Aman Ahmad.  
 

2. MECHANISM OF ACTION  
 
An oral, selective, and reversible JAK inhibitor is 
called baricitinib. The tyrosine-protein kinase 
family of intracellular enzymes, JAK, regulates 
signals from growth factor receptors and 
cytokines that are important for immune cell 
activity [5,15] concluded by et al Anam Ahmad, 
Amanda Mogul Four JAK proteins—TYK2, JAK1, 
JAK2, and JAK 3—form distinct pairings in 
different cell receptors to produce homodimers or 
heterodimers. These JAK dimers stimulate 
intracellular activity, including the transcription of 
inflammatory mediator genes, by 
phosphorylating the STAT proteins. This 
ultimately sets off an autoimmune reaction [5,16] 
concluded by et al Anam Ahmad, Musumeci, 
Francesca.  
 
There is an increased affinity of baricitinib for 
JAK1 and JAK2. The medication works by 
blocking these JAK proteins, which stop STATs 

from becoming phosphorylated and activated. 
Furthermore, baricitinib modifies the signaling 
pathway of certain growth factors, interleukins, 
and interferons. Additionally, baricitinib causes 
cell death and reduces the growth of JAK1/JAK2 
expression in mutant cells. Within one week of 
starting therapy, baricitinib dramatically lowered 
blood C-reactive protein levels in rheumatoid 
arthritis patients.  

 
Alopecia areata is thought to be                             
caused by a confluence of immunological 
dysregulation and hereditary factors. Important 
cytokines that depend on JAKs for intracellular 
signaling, like interleukin-15 and interferon-γ, are 
implicated in the illness process. Baricitinib has 
proven to be beneficial in helping people with 
severe alopecia areata regrow their hair [5,17] 
concluded by et al Anam Ahmad. Brett King, 
M.D., Ph.D.  

 
3. PHARMACOKINETICS  
 
Absorption: Baricitinib has a 97% bioavailability 
and is quickly absorbed from the gastrointestinal 
tract. Baricitinib takes an average of 1.5 hours to 
reach peak plasma concentration, although it can 
take anywhere from 0.5 to 3 hours. It has not 
been demonstrated that administering food alters 
the peak plasma concentration.  

 
Distribution: Approximately 50% of baricitinib 
can bind to plasma proteins. Baricitinib's 
apparent volume of distribution is 76 L, which 
suggests that the medication is widely distributed 
throughout the body's tissues.  

 
Metabolism: The hepatic metabolism of 
approximately 10% of the medication occurs 
through oxidation by the CYP3A4(cytochrome 
p450 3A4) enzyme and organic anion 
transporter-3 (OAT3). The strong OAT3 inhibitor 
probenecid causes a two-fold rise in blood levels 
of baricitinib. Consequently, patients taking 
probenecid at the same time should cut their 
baricitinib dosage in half [5] concluded by et al 
Anam Ahmad. 

 
Elimination: In clinical pharmacology trials, the 
gastrointestinal tract eliminates 20% of the 
medication, and the kidneys clear about 75% of 
it. In patients with rheumatoid arthritis, baricitinib 
has an approximately 12-hour elimination half-life 
and a renal clearance of about 12 L/h [5,18] 
concluded by et al Anam Ahmad. Jack G. Shi 
PhD.  



 
 
 
 

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4. ADMINISTRATION  
 

4.1 Available Dosage Forms and 
Strengths  

 
Oral administration of baricitinib is possible in 
two dosage forms: 2 mg and 4 mg. For 
rheumatoid arthritis, a dose of 2 mg taken once 
daily by mouth is advised. Clinical trials 
evaluated the effects of 2 mg oral baricitinib in 
conjunction with 10–14 days of antiviral 
medication in the setting of COVID-19 infection 
[19] concluded by et al Feng Huang. 
 

4.2 Adult Dosage 
  
For rheumatoid arthritis, 2 mg of                          
baricitinib taken orally once daily, with or                 
without food, is the suggested dosage. The 
medication can be taken either alone or in 
conjunction with methotrexate or non-biologic 
DMARDs.  
 
COVID-19: The National Institutes of Health 
advises against using baricitinib as a secondary 
immunomodulatory medication and in favor of 
dexamethasone in COVID-19 patients who are 
exhibiting rapidly increasing oxygen 
requirements and systemic inflammation. Adults 
should take 4 mg of baricitinib once a day for a 
period of 14 days, or until they are released from 
the hospital [20] concluded by et al S Honda, M 
Harigai.  
 

4.3 Adverse Effects  
 
Baricitinib is generally regarded as a safe and 
well-tolerated drug. However, its 
immunosuppressive qualities raise the risk of 
serious infections. The most common adverse 
events recorded in alopecia areata patients 
throughout clinical trials were upper respiratory 
tract infections, acne vulgaris, headaches, 
urinary tract infections, and folliculitis                      
[21,22] concluded by et al Egídio Freitas, T 
Bieber, N Katoh. Herpes zoster infections are 
also on the rise. Baricitinib has been linked to 
bone marrow suppression and hematological 
abnormalities such as anemia, neutropenia, and 
lymphopenia and should be monitored regularly 
in the lab. Another side effect commonly seen 
after 12 weeks of baricitinib treatment is an 
increase in mean cholesterol, low-density 
lipoprotein (LDL), and high-density lipoprotein 
(HDL) levels without an increase in the LDL to 
HDL ratio. Furthermore, some individuals may 
have a rise in creatine phosphokinase levels 

[23,24] concluded by et al D Van Der Heijde, 27 
PC Taylor.  
 

4.4 Baricitinib for the Treatment of 
Rheumatoid Arthritis  

 
Since the mid-1990s, the treatment approach to 
rheumatoid arthritis has undergone significant 
modifications in the area of rheumatology. With 
the increased use of traditional synthetic 
DMARDs, the advent of biologic treatments, and, 
most recently, the development of novel small 
compounds that target the JAK pathway, 
treatment paradigms have changed. A strong 
and specific JAK1 and JAK2 inhibitor is 
baricitinib. It has been proposed that various 
medicines may exhibit differential clinical effects 
based on their profiles of JAK inhibition [25,26] 
concluded by et al Mark C. Genovese, M.D., Joel 
Kremer, M.D., Omid Zamani, M.D., JJ O'Shea, J 
Israel, H Hakobyan.  
 
Adults with mild to severe active RA are advised 
to take baricitinib once a day. It is usually 
administered as a second-choice                      
medication after patients have tried using TNF 
inhibitors but did not experience meaningful relief 
or could not handle the medication owing to 
adverse effects because of several                     
potentially dangerous side effects.Both brands 
warn of potential significant adverse effects. Both 
caution against administering the medicine if 
there is a known severe illness, such as 
tuberculosis (TB), and recommend TB screening 
prior to therapy. Other adverse effects may 
include kidney, cardiovascular, and eye health 
[27,28] concluded by et al Ivan Urits1, Jacob 
Israel2.  
 
Since the mid-1990s, the treatment approach for 
rheumatoid arthritis has changed dramatically. 
Treatment paradigms have shifted with the 
increased use of traditional synthetic DMARDs, 
the advent of biologic medicines, and, most 
recently, novel small compounds targeting the 
JAK pathway. Baricitinib is a very effective and 
specific inhibitor of JAK1 and JAK2. It has been 
proposed that medicines with varied JAK 
inhibition profiles may have unique clinical 
outcomes.  
 
The purpose of this evaluation was to evaluate 
the safety and effectiveness of baricitinib in 
patients with active rheumatoid arthritis who 
were using conventional synthetic DMARDs but 
had not responded adequately to earlier biologic 
DMARD therapy. In this patient cohort, once-



 
 
 
 

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daily oral baricitinib resulted in substantial clinical 
improvements at 12 weeks when compared to 
placebo. The therapeutic advantages were 
greater with the 4 mg dosage than with the 2 mg 
dose. Adverse events, such as non-serious 
infections, were more common in the baricitinib 
group than in the placebo group. Baricitinib was 
associated with lower neutrophil counts, higher 
creatinine levels, and higher low-density 
lipoprotein cholesterol levels. These adjustments 
were primarily modest and did not result in their 
removal from the research [25] concluded by et 
al Mark C. Genovese, M.D., Joel Kremer, M.D., 
Omid Zamani, M.D.  
 

4.5 Efficacy of Baricitinib in Phase II 
Studies  

 
In the JADA(Journal of the American Dental 
Association) research (phase 2), 301 patients 
with active RA(rheumatoid arthritis) receiving 
steady-state MTX and MTX-IR were included. At 
week 12, 76% of patients in the combined 
baricitinib 4 and 8 mg group had an 
ACR20(American college of Rheumatology 20) 
[29] concluded by et al David T. Felson MD, 
MPH, response, compared to 41% in the placebo 
group [30] concluded by et al David T. Felson 
MD, MPH. The placebo and 4 mg groups 
showed significant differences in secondary 
endpoints, including minimal disease activity and 
remission. The JADA(Journal of the American 
Dental Association) research (phase 2) included 
145 Japanese patients with active RA and MTX-
IR(methotrexate) receiving steady background 
MTX. At week 12, the combined baricitinib 4 mg 
and 8 mg group had a significantly greater 
ACR20 response rate (77%) than the placebo 
group (31%), according to a primary efficacy 
study [31] concluded by et al Yoshiya Tanaka. At 
week 12, the 2, 4, and 8 mg groups improved 
similarly across efficacy measures. However, the 
4 and 8 mg groups showed earlier onset than the 
1 and 2 mg groups as early as week 2 [1] 
concluded by et al Satoshi Kubo.  
 

4.6 Efficacy of Baricitinib in Phase III 
Studies  

 
Six phase 3 trials on baricitinib for RA are 
underway or completed to establish its efficacy, 
evaluate adverse effects, and compare it to other 
DMARDs or placebos. In these investigations, 
patients in both the baricitinib and control groups 
received corticosteroids at baseline. Baricitinib 
should be compared to MTX with corticosteroids, 
as early RA patients typically get both 

medications. However, no trials have compared 
baricitinib to MTX with corticosteroids [1] 
concluded by et al Satoshi Kubo.  
 
The RA-BEACON trial (JADE(JAK1 Atopic 
Dermatitis Efficacy and Safety) comprised 527 
individuals with active RA and TNF-IR(tumor 
necrosis factor) . At week 12, 55% of patients 
who received the 4 mg dosage of baricitinib had 
an ACR20 response, compared to 27% who 
received the placebo [32] concluded by et al 
Charles Ludivico, M.D. Compared to the 
placebo, there were substantial improvements in 
the SDAI(simple Disease Activity Index) ≤3.3 
ratio. Downloaded by [Weill Cornell Medical 
College] at 06:35 on July 20, 2016. Week 24 for 
the baricitinib 4 mg group. All subgroup analyses 
showed a favorable treatment impact, regardless 
of prior bDMARD usage (number or kind) [33] 
concluded by et al Dario Ummarino.  

 
4.7 Safety and Tolerability of Baricitinib  
 
In the RA-BEACON study [32], concluded by etal 
Charles Ludivico, M.D. 527 adult patients with 
moderately to severely active RA who had not 
responded to or were intolerant to at least one 
biologic TNF-α inhibitor and were taking 
background csDMARD therapy experienced 
more treatment-emergent adverse events 
(TEAEs) than those taking placebo. Patients 
receiving the 2 mg and 4 mg doses of baricitinib 
experienced more adverse events (71%) and 
77%, respectively, compared to those receiving 
the placebo (64%), including infections (44% and 
40%, vs. 31%). Mild upper respiratory tract 
infections were found to significantly lead to 
imbalances. The baricitinib group saw briefer, 
transitory disruptions of the study medicine. SAE 
rates were 4%, 10%, and 7% for the three 
groups, respectively. The proportion of patients 
experiencing an SAE was consistent across 
treatment groups. There were only two non-
melanoma skin tumors in the baricitinib 4 mg 
group, with no reports of solid organ, 
hematologic, or other malignancies. The trial 
found two treatment-emergent serious adverse 
cardiovascular events (MACE): one myocardial 
infarction (baricitinib 4 mg) and one basilar artery 
thrombosis (baricitinib 4 mg), which also resulted 
in one death. No patients had a gastrointestinal 
perforation.Serum creatinine and LDL cholesterol 
levels increased, and neutrophil counts 
somewhat decreased when baricitinib was 
administered. In the baricitinib groups, very few 
patients experienced a treatment-emergent 
laboratory abnormality that led to a permanent 



 
 
 
 

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discontinuation of the study medicine [1] 
concluded by et al Satoshi Kubo. 
 

5. CONCLUSION 
 
In the review, we have described the potential of 
the JAK inhibitor baricitinib. Baricitinib has 
demonstrated a greater selectivity for JAK1 and 
JAK2 than for the other tyrosine kinases, JAK3 
and Tyk2, in basic research investigations, 
suggesting that it may be useful as a molecular 
target medication. The use of baricitinib in RA is 
supported by strong evidence, particularly when 
combined with the existing DMARD treatment.  
 
DISCLAIMER (ARTIFICIAL INTELLIGENCE) 
 
Author(s) hereby declare that NO generative AI 
technologies such as Large Language Models 
(ChatGPT, COPILOT, etc) and text-to-image 
generators have been used during writing or 
editing of manuscripts.  
 

COMPETING INTERESTS 
 
Authors have declared that no competing 
interests exist. 
 

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