Jaktinib (DB17545): A Comprehensive Pharmacological and Clinical Monograph of a Novel Dual JAK/ACVR1 Inhibitor

Executive Summary

Jaktinib (DrugBank ID: DB17545) is an orally administered small molecule Janus kinase (JAK) inhibitor developed by Suzhou Zelgen Biopharmaceuticals. Chemically, it is a deuterated analog of momelotinib, a strategic modification intended to optimize its pharmacokinetic profile. Jaktinib's primary mechanism of action involves the inhibition of the JAK-STAT signaling pathway, a critical mediator of cellular processes in hematopoiesis and immunity. It exhibits a distinct inhibitory profile with potent activity against JAK2 and TYK2. Critically, Jaktinib also inhibits Activin A receptor, type 1 (ACVR1), a key regulator of hepcidin and iron metabolism. This dual mechanism confers a unique clinical profile, enabling the simultaneous management of myeloproliferation, constitutional symptoms, and disease-related anemia—a significant challenge in the treatment of myelofibrosis (MF).

The clinical development program for Jaktinib has demonstrated robust efficacy and a manageable safety profile across a range of hematologic and inflammatory conditions. In May 2025, Jaktinib was approved by China's National Medical Products Administration (NMPA) for the treatment of intermediate- to high-risk myelofibrosis. This approval was based on the pivotal Phase III ZGJAK016 trial, in which Jaktinib demonstrated statistically significant superiority over the standard-of-care agent hydroxyurea in reducing spleen volume, while also showing improvements in constitutional symptoms and anemia with a more favorable hematologic safety profile. Furthermore, Jaktinib has shown significant clinical activity in patients with MF who are intolerant, refractory, or have relapsed after treatment with ruxolitinib.

Beyond hematology, Jaktinib is in late-stage clinical development for several autoimmune and inflammatory disorders. It has completed Phase III trials and has been submitted for regulatory approval in China for alopecia areata. Phase III trials are actively recruiting for atopic dermatitis and ankylosing spondylitis, following positive Phase II results. The safety profile of Jaktinib is consistent with the JAK inhibitor class, with hematological toxicities being the most common dose-limiting adverse events; however, its profile appears favorable when compared directly to hydroxyurea. While subject to the class-wide safety considerations regarding major adverse cardiovascular events, thrombosis, and malignancy, short-term studies have not revealed an elevated signal for these events. Jaktinib's unique dual-target mechanism, particularly its anemia-mitigating effects, positions it as a differentiated and potentially paradigm-shifting therapeutic agent in the management of myelofibrosis and a promising candidate for a range of inflammatory diseases.

Introduction and Drug Identification

Overview and Drug Classification

Jaktinib is an investigational small molecule drug classified as a Janus kinase (JAK) inhibitor.[1] Developed by Suzhou Zelgen Biopharmaceuticals, a company based in Kunshan, Jiangsu, China, Jaktinib represents a new entrant in the class of targeted synthetic disease-modifying drugs.[2] Its development program has explored both systemic and localized therapeutic applications, with formulations including oral tablets for systemic diseases and a topical cream for dermatological conditions.[5] During its development, the compound has been referred to by several synonyms, including Gecaxitinib, Jakotinib hydrochloride, and Gecacitinib, a common practice for investigational drugs that necessitates careful tracking across scientific literature and clinical trial databases.[1]

Chemical Properties and Structural Analysis

Jaktinib is defined by a unique chemical structure and a specific set of identifiers that distinguish it from other molecules. Its molecular formula is C23​H18​D4​N6​O2​, with a molar mass of 418.491 g·mol−1.[1] The "D4" in the formula signifies the presence of four deuterium atoms, a key structural feature.

The compound is explicitly identified as a deuterated analog of momelotinib, another established JAK inhibitor.[1] Specifically, Jaktinib is Momelotinib-3,3,5,5-d4, indicating that four hydrogen atoms on the morpholine ring of the momelotinib molecule have been strategically replaced with deuterium, a stable, non-radioactive isotope of hydrogen.[11] This modification is a deliberate pharmaceutical strategy known as "deuterium switching" or leveraging the "kinetic isotope effect." The rationale behind this chemical alteration is to improve the drug's metabolic stability. The carbon-deuterium (C-D) bond is stronger than the carbon-hydrogen (C-H) bond, making it more resistant to cleavage by metabolic enzymes, such as those in the cytochrome P450 family. This modification is intended to alter the drug's pharmacokinetic properties—potentially slowing its rate of metabolism and clearance—without changing its fundamental pharmacodynamic activity at the target site.[9] The anticipated result is a more favorable pharmacokinetic profile, which could manifest as a longer half-life, more stable plasma concentrations between doses, and potentially a reduced dosing frequency or total dose, thereby enhancing both safety and patient adherence. This strategic design is a key differentiator when evaluating Jaktinib in the context of its parent compound and other drugs in its class. Patent documents confirm its molecular structure and its classification as an inhibitor of non-receptor tyrosine kinases, including JAK kinases, for the treatment of myeloproliferative diseases and inflammatory conditions.[12]

Table 1: Key Chemical and Physical Properties of Jaktinib

Property	Value	Source(s)
Generic Name	Jaktinib	2
Alternative Names	Gecaxitinib, Gecacitinib, Jakotinib hydrochloride	1
DrugBank ID	DB17545	1
CAS Number	1619927-66-0	1
Molecular Formula	C23​H18​D4​N6​O2​	1
Molar Mass	418.491 g·mol−1	1
IUPAC Name	N-(cyanomethyl)-4-{2-[4-(3,3,5,5-tetradeuteriomorpholin-4-yl)anilino]pyrimidin-4-yl]}benzamide	1
SMILES	[2H]C1([2H])COCC([2H])([2H])N1c1ccc(Nc2nccc(-c3ccc(C(=O)NCC#N)cc3)n2)cc1	1
InChIKey	ZVHNDZWQTBEVRY-RYIWKTDQSA-N	1

Mechanism of Action and Pharmacodynamics

The JAK-STAT Signaling Pathway: A Foundational Overview

The therapeutic activity of Jaktinib is rooted in its ability to modulate the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway. This pathway is a fundamental intracellular signaling cascade that serves as a rapid communication route from the cell surface to the nucleus.[13] It is activated by a wide array of extracellular cytokines, such as interleukins and interferons, as well as growth factors. These ligands bind to specific transmembrane receptors, triggering the activation of receptor-associated JAK enzymes.[15]

The JAK family in mammals comprises four non-receptor tyrosine kinases: JAK1, JAK2, JAK3, and tyrosine kinase 2 (TYK2).[13] Upon activation, JAKs phosphorylate tyrosine residues on the receptor's intracellular domain, creating docking sites for STAT proteins. STATs are then recruited and subsequently phosphorylated by the JAKs, leading to their dimerization and translocation into the nucleus. Once in the nucleus, STAT dimers bind to specific DNA sequences to regulate the transcription of target genes.[15] This signaling cascade is essential for numerous physiological processes, including hematopoiesis, immune cell development and function, inflammation, cell proliferation, and apoptosis.[13] Pathological dysregulation of the JAK-STAT pathway is a key driver in the pathogenesis of various diseases, including myeloproliferative neoplasms (MPNs) like myelofibrosis and a broad spectrum of autoimmune and inflammatory disorders, such as alopecia areata and axial spondyloarthritis.[13]

Primary Target Profile: Inhibition of Janus Kinases

Jaktinib functions as a potent, small-molecule inhibitor of the JAK family of enzymes.[2] By binding to the ATP-binding site of these kinases, Jaktinib prevents their activation and the subsequent phosphorylation cascade involving the STAT proteins.[19] This blockade effectively disrupts the downstream signaling that promotes abnormal cell proliferation and survival in malignant cells and mediates the pro-inflammatory cytokine signaling characteristic of autoimmune diseases.[19]

While some sources broadly classify Jaktinib as an inhibitor of JAK1, JAK2, and JAK3, more detailed pharmacological characterizations suggest a degree of selectivity.[2] It appears to exhibit more potent inhibitory activity against JAK2 and TYK2, with comparatively lesser effects on JAK3 and minimal activity against JAK1.[4] This specific inhibitory profile is a hallmark of more recently developed JAK inhibitors and can influence both the efficacy and safety profile of the drug. The strong inhibition of JAK2 is central to its therapeutic effect in myelofibrosis, a disease often driven by a gain-of-function mutation in JAK2 (JAK2V617F) that leads to constitutive activation of the JAK-STAT pathway.[9]

Key Secondary Target: The Role of ACVR1 Inhibition in Anemia

A critical and differentiating feature of Jaktinib's mechanism is its inhibitory activity against a secondary target: Activin A receptor, type 1 (ACVR1), also known as ALK2.[8] This property is inherited from its parent compound, momelotinib, which is also a known ACVR1 inhibitor.[10] The ACVR1 signaling pathway is a central regulator of iron homeostasis through its control of hepcidin, a peptide hormone that governs iron absorption and recycling. In chronic inflammatory states like myelofibrosis, elevated levels of inflammatory cytokines lead to increased hepcidin production. This, in turn, sequesters iron, rendering it unavailable for erythropoiesis (red blood cell production) and leading to the "anemia of chronic inflammation".[21]

By inhibiting ACVR1, Jaktinib suppresses the signaling that leads to hepcidin production. The resulting decrease in circulating hepcidin levels releases iron stores, making iron available for incorporation into hemoglobin and effectively stimulating red blood cell production.[21] This dual mechanism of action is of profound clinical significance. While the inhibition of the JAK-STAT pathway addresses the core myeloproliferative aspects of MF—such as splenomegaly and constitutional symptoms—the concurrent inhibition of ACVR1 directly counteracts one of the disease's most debilitating and prognostically negative features: anemia. This contrasts sharply with first-generation JAK inhibitors like ruxolitinib, which are highly effective against splenomegaly and symptoms but can often exacerbate anemia through myelosuppression.[27] The ability of Jaktinib to provide a "triple benefit"—controlling spleen size, alleviating symptoms, and improving anemia—with a single molecule represents a major therapeutic advance and positions it uniquely within the treatment landscape for myelofibrosis.

Clinical Pharmacology and Pharmacokinetics (PK)

A Phase I, randomized, double-blind, placebo-controlled study in 126 healthy Chinese volunteers provided the foundational pharmacokinetic data for Jaktinib, characterizing its absorption, distribution, metabolism, and excretion (ADME) profile.[6]

Absorption

Following oral administration, Jaktinib is absorbed with a median time to reach peak plasma concentration (Tmax​) ranging from 1.25 to 3.5 hours, indicating relatively rapid absorption.[29] A significant food effect was observed; administration with a high-fat breakfast substantially increased drug exposure. Peak concentration (

Cmax​) increased by 2.6-fold and the total exposure (Area Under the Curve, AUC) increased by 2.28-fold compared to administration in a fasted state. The presence of food also delayed absorption, prolonging the median Tmax​ from 2 hours to 4 hours.[6] This pronounced food effect necessitates consistent administration relative to meals to ensure predictable drug exposure and avoid significant variability in clinical response and safety.

Distribution

Jaktinib demonstrates extensive distribution throughout the body, as evidenced by a large apparent volume of distribution (Vz​/F) ranging from 533 to 1033 L.[28] This suggests that the drug does not remain confined to the bloodstream but penetrates widely into tissues.

Metabolism

The biotransformation of Jaktinib occurs primarily through oxidation and hydrolysis pathways. This process yields two main metabolites identified as ZG0244 (formed by oxidation) and ZG0245 (formed by hydrolysis).[6] ZG0244 is the most abundant metabolite in circulation and its plasma concentration profile closely mirrors that of the parent drug. In contrast, ZG0245 appears more slowly in the plasma and, unlike the parent drug or ZG0244, it demonstrates moderate accumulation with repeated dosing, with an accumulation ratio (

Rac​) of 2.252–5.286.[28] The potential pharmacological activity of this accumulating metabolite could contribute to the drug's sustained efficacy but also warrants monitoring for potential delayed toxicity.

Excretion

The primary route of elimination for Jaktinib and its metabolites is via the feces.[6] The overall recovery of the administered dose in urine and feces is relatively low, with the accumulated fraction of the parent drug and its measured metabolites accounting for only 19.478% of the dose.[29] This suggests that other unmeasured metabolites or elimination pathways may contribute to the drug's clearance.

Elimination Half-Life

The elimination half-life (t1/2​) for the parent Jaktinib molecule ranges from 2.952 to 9.040 hours.[29] The metabolite ZG0245 has a substantially longer half-life, ranging from 8.08 to 24.549 hours, which is consistent with its observed accumulation upon multiple dosing.[28]

Dose Proportionality and Potential Drug-Drug Interactions

Jaktinib exhibits linear pharmacokinetics, with both Cmax​ and AUC increasing proportionally with single doses ranging from 25 mg to 400 mg.[6] No significant accumulation of the parent drug was observed after 10 days of continuous dosing.[6]

While specific drug-drug interaction (DDI) studies for Jaktinib are not fully detailed, its profile as a JAK inhibitor suggests a high potential for interactions involving the cytochrome P450 (CYP) enzyme system. JAK inhibitors as a class are often metabolized by CYP3A4, CYP2C19, and/or CYP2C9.[32] Therefore, co-administration of Jaktinib with strong inhibitors of these enzymes (e.g., ketoconazole, fluconazole) would be expected to increase Jaktinib plasma concentrations, potentially raising the risk of toxicity. Conversely, co-administration with strong CYP inducers (e.g., rifampin) could decrease Jaktinib exposure and compromise efficacy.[32] Dose adjustments will likely be required when used with such agents. Interactions with drug transporters, such as Organic Anion Transporter 3 (OAT3), are also a consideration for this drug class.[32]

Table 2: Summary of Phase I Pharmacokinetic Parameters in Healthy Volunteers

Parameter	Value / Observation	Source(s)
Time to Peak Concentration (Tmax​)	1.25–3.5 hours (fasted)	28
Peak Concentration (Cmax​)	Dose-proportional (25-400 mg)	29
Total Exposure (AUC)	Dose-proportional (25-400 mg)	29
Elimination Half-Life (t1/2​)	Parent: 2.952–9.040 hours Metabolite ZG0245: 8.08–24.549 hours	28
Volume of Distribution (Vz​/F)	533–1033 L	28
Accumulation Ratio (Rac​)	Parent: ~1.0 Metabolite ZG0245: 2.252–5.286	28
Food Effect (High-Fat Meal)	Cmax​ ↑ 2.6-fold AUC ↑ 2.28-fold	28

Clinical Development and Efficacy in Myeloproliferative Neoplasms

Overview of the Myelofibrosis (MF) Clinical Program

Jaktinib has been systematically evaluated in a comprehensive clinical program for patients with intermediate- or high-risk myelofibrosis (MF), a group of myeloproliferative neoplasms that includes primary myelofibrosis (PMF), post-polycythemia vera MF (post-PV-MF), and post-essential thrombocythemia MF (post-ET MF).[3] The program was designed to assess the drug's utility across the entire clinical spectrum of the disease, enrolling JAK inhibitor-naïve patients as well as those with advanced disease who were intolerant to or had become refractory or relapsed after treatment with the first-in-class JAK inhibitor, ruxolitinib.[36]

Pivotal Phase III Trial in JAKi-Naïve Patients (ZGJAK016 / NCT04617028)

The cornerstone of Jaktinib's approval for myelofibrosis was the ZGJAK016 trial, a multicenter, randomized (2:1), double-blind, active-controlled Phase III study conducted across 38 centers in China.[25] The trial enrolled 105 adult patients with intermediate-2 or high-risk MF and compared the efficacy and safety of Jaktinib, administered at 100 mg twice daily (BID), against hydroxyurea (HU), a commonly used standard-of-care agent.[40]

The primary endpoint was the proportion of patients achieving a spleen volume reduction of 35% or more from baseline (SVR35) at week 24, as assessed by MRI or CT imaging. The trial successfully met this endpoint, with Jaktinib demonstrating statistically significant and clinically meaningful superiority over hydroxyurea. Final results showed an SVR35 rate of 64.8% in the Jaktinib arm compared to just 26.5% in the hydroxyurea arm (p=0.0002).[25] Interim results presented earlier were consistent with this finding, showing an SVR35 rate of 72.3% for Jaktinib versus 17.4% for hydroxyurea (

p≤0.0001).[40]

Secondary endpoints further supported Jaktinib's superior clinical profile. A strong positive trend was observed for symptom improvement, with 63.8% of patients on Jaktinib achieving a 50% or greater reduction in their Total Symptom Score (TSS50), compared to 43.5% of those on hydroxyurea (p=0.1163).[40] Most notably, reflecting its dual mechanism of action, Jaktinib demonstrated a clear benefit in managing anemia. Among non-transfusion-dependent patients, 31% treated with Jaktinib achieved a clinically significant hemoglobin increase of

≥20 g/L, more than double the rate of 15% seen in the hydroxyurea group.[25]

Phase II Studies in Ruxolitinib-Experienced Populations

To establish its role in later lines of therapy, Jaktinib was evaluated in two key Phase II studies targeting patients who could no longer benefit from ruxolitinib.

In a single-arm, open-label Phase 2b study (NCT04217993), 51 patients who were intolerant to ruxolitinib (defined by the development of significant hematological toxicities or an increased need for transfusions) were treated with Jaktinib 100 mg BID.[22] The study met its primary endpoint, with 43.2% of evaluable patients achieving SVR35 at week 24.[22] The best SVR35 rate at any time during the study was 54.5%. Significant improvements were also seen in symptom burden (61.8% TSS50 rate) and anemia, where 41.9% of transfusion-independent patients with low baseline hemoglobin experienced a

≥20 g/L increase.[37]

A separate Phase II trial (NCT04851535) enrolled 34 patients who were refractory to or had relapsed after ruxolitinib treatment, representing a population with high unmet need.[38] In this challenging setting, Jaktinib 100 mg BID still demonstrated substantial clinical activity. The SVR35 rate at week 24 was 32.4%, and 46.4% of patients achieved a TSS50 response.[38] The anemia benefit was particularly pronounced, with 50% of eligible patients achieving a

≥20 g/L hemoglobin increase.[38]

Long-Term Efficacy and Survival Data (ZGJAK002 / NCT03886415)

The ZGJAK002 trial provided crucial long-term data on Jaktinib in 118 JAKi-naïve patients, comparing two dosing regimens: 100 mg BID versus 200 mg once daily (QD).[23] The results favored the 100 mg BID regimen, which demonstrated a numerically higher best spleen response rate (69.7% vs. 46.2%) and was subsequently selected for Phase III development.[24] Long-term follow-up with a median of 30.7 months showed that these responses were durable, with over 50% of patients in both arms maintaining their spleen response at 120 weeks. Encouragingly, the 36-month survival rates were 78.2% for the BID group and 73.6% for the QD group, suggesting a potential long-term survival benefit.[24]

The collective evidence from this comprehensive clinical program establishes a unique therapeutic profile for Jaktinib that could shift the treatment paradigm in myelofibrosis. Unlike ruxolitinib, which effectively manages spleen and symptoms but often at the cost of worsening anemia, Jaktinib addresses all three cardinal features of the disease. Its demonstrated superiority over hydroxyurea in the front-line setting, combined with its profound "triple benefit" in the difficult-to-treat second-line population, positions it as a versatile agent. By proactively managing anemia through its ACVR1 inhibitory activity, Jaktinib may allow for more consistent and optimal dosing, potentially leading to more durable disease control and improved long-term outcomes. This integrated approach offers a more holistic treatment strategy, simplifying management for clinicians and potentially improving the overall prognosis for patients with myelofibrosis.

Table 3: Summary of Efficacy Results from Key Myelofibrosis Clinical Trials

Trial ID (Patient Population)	Comparator	Primary Endpoint	SVR35 Rate (%)	TSS50 Rate (%)	Anemia Response (%)*	Source(s)
ZGJAK016 (JAKi-Naïve)	Hydroxyurea	SVR35 at Wk 24	64.8 vs. 26.5	63.8 vs. 43.5	31.0 vs. 15.0	25
NCT04217993 (RUX-Intolerant)	Single-Arm	SVR35 at Wk 24	43.2	61.8	41.9	37
NCT04851535 (RUX-Refractory)	Single-Arm	SVR35 at Wk 24	32.4	46.4	50.0	38
*Anemia response defined as proportion of transfusion-independent patients with baseline hemoglobin ≤100 g/L achieving a ≥20 g/L increase.

Clinical Efficacy in Inflammatory and Autoimmune Disorders

Leveraging a mechanism of action validated across numerous immune-mediated diseases, Suzhou Zelgen Biopharmaceuticals is pursuing a broad, multi-indication development strategy for Jaktinib, mirroring the successful expansion of other JAK inhibitors. This approach indicates a high degree of confidence in the drug's core ability to modulate the pathological inflammation driving conditions in rheumatology and dermatology, aiming to maximize its therapeutic and commercial potential.

Ankylosing Spondylitis (Axial Spondyloarthritis, axSpA)

Jaktinib has shown significant promise in the treatment of active radiographic axial spondyloarthritis (r-axSpA). A Phase II, multicenter, randomized, double-blind, placebo-controlled trial (NCT04507659) enrolled 107 patients who had an inadequate response to non-steroidal anti-inflammatory drugs (NSAIDs).[3] Patients were randomized to receive Jaktinib 75 mg BID, Jaktinib 100 mg BID, or a placebo for 16 weeks.

The trial met its primary and key secondary endpoints, demonstrating a clear therapeutic benefit for Jaktinib. For the primary endpoint, the Assessment of SpondyloArthritis international Society 20 (ASAS20) response at week 16, rates were 57.1% for the 75 mg group and 61.1% for the 100 mg group, both significantly higher than the 33.3% rate in the placebo group.[3] A similar dose-dependent response was observed for the more stringent ASAS40 endpoint, with rates of 37.1% (75 mg) and 47.2% (100 mg) for Jaktinib, compared to 13.9% for placebo.[3] Based on these positive results, Phase III trials for this indication are currently recruiting, signaling a strong commitment to pursuing approval in this therapeutic area.[2]

Alopecia Areata (AA)

Jaktinib has undergone a comprehensive clinical program for alopecia areata, an autoimmune disorder characterized by T-cell-mediated attack on hair follicles.[18] This pathological process is heavily dependent on cytokine signaling through the JAK-STAT pathway, making it an ideal target for JAK inhibitors. The development program has successfully completed Phase II (NCT04034134) and Phase III trials (NCT05051761, NCT05255237).[52] The program has advanced to the preregistration phase in China, with a New Drug Application (NDA) or Biologics License Application (BLA) having been submitted to the NMPA for regulatory review and potential marketing approval.[3]

Atopic Dermatitis (AD)

Recognizing the significant role of JAK-STAT signaling in the pathogenesis of atopic dermatitis, Jaktinib is being developed in both oral tablet and topical cream formulations to address this condition.[5] Following the completion of initial Phase I/II trials, the program has advanced into large-scale Phase III studies.[7] Multiple Phase III trials (NCT05676242, NCT05526222) are actively recruiting patients with moderate-to-severe atopic dermatitis, representing a major area of investment and a key part of the drug's expansion strategy into dermatology.[2]

Other Investigational Indications

The clinical development pipeline for Jaktinib includes several other indications at various stages:

• Plaque Psoriasis: A Phase II trial (NCT04612699) in patients with moderate-to-severe plaque psoriasis has been completed.[57]
• Graft-versus-Host Disease (GVHD): The drug is in late-stage development in China, with Phase III trials for acute GVHD and Phase II for steroid-refractory GVHD.[3]
• Idiopathic Pulmonary Fibrosis (IPF): A Phase II trial has been completed.[2]
• Vitiligo: Jaktinib is currently in Phase II development for this autoimmune skin pigmentation disorder.[8]
• Discontinued Programs: Demonstrating a strategic focus on the most promising areas, development programs for COVID-19 pneumonia, systemic lupus erythematosus, and certain other cancers have been discontinued.[8]

Comprehensive Safety and Tolerability Profile

Overview of Adverse Events from Clinical Trials

Across its extensive clinical program, Jaktinib has demonstrated a generally acceptable safety and tolerability profile.[3] In the initial Phase I study conducted in healthy volunteers, the most frequently reported treatment-related adverse events (TRAEs) were neutropenia, diarrhea, dizziness, and headache, with the majority being mild in severity.[6] In the placebo-controlled Phase II trial for axial spondyloarthritis, the overall incidence of treatment-emergent adverse events (TEAEs) was comparable between the Jaktinib-treated groups (88.6% to 94.4%) and the placebo group (86.1%), suggesting that at the doses studied, the drug did not significantly increase the overall rate of adverse events over a 16-week period.[3]

Hematological Adverse Events

As is characteristic of inhibitors targeting JAK2, the most clinically significant and common Grade ≥3 adverse events associated with Jaktinib are hematological. The drug's safety profile in this regard appears to be a key differentiator.

• In JAKi-Naïve Myelofibrosis (vs. Hydroxyurea): In the pivotal ZGJAK016 trial, Jaktinib exhibited a more favorable hematologic safety profile compared to the active comparator, hydroxyurea. Rates of Grade ≥3 TEAEs were notably lower for Jaktinib, including anemia (26.8% vs. 44.1%), thrombocytopenia (15.5% vs. 32.4%), and neutropenia (1.4% vs. 20.6%).[25] This superior hematologic safety, particularly the lower incidence of severe anemia, is a significant clinical advantage.
• In Ruxolitinib-Intolerant Myelofibrosis: In patients who had discontinued ruxolitinib due to intolerance (primarily hematological), the most common Grade ≥3 TEAEs with Jaktinib were anemia (31.1%), thrombocytopenia (22.2%), and neutropenia (15.6%).[27]
• In Ruxolitinib-Refractory Myelofibrosis: In this heavily pre-treated population, the most frequent Grade ≥3 TEAEs were thrombocytopenia (32.4%) and anemia (32.4%).[38]

This safety profile suggests a distinct clinical advantage. The primary dose-limiting toxicities of first-generation JAK inhibitors like ruxolitinib are myelosuppressive, often leading to dose reductions that can compromise efficacy.[27] Jaktinib's ability to demonstrate superiority over hydroxyurea with lower rates of severe cytopenias in a head-to-head trial is a powerful finding.[25] This favorable profile, likely resulting from the combination of its specific JAK selectivity and anemia-mitigating ACVR1 inhibition, may allow clinicians to maintain optimal therapeutic dosing more consistently, potentially leading to better long-term outcomes without the same safety trade-offs.

Non-Hematological Adverse Events of Interest

The most common non-hematological adverse events are consistent with the known effects of JAK inhibition.

• Infections: Due to their immunomodulatory mechanism, JAK inhibitors carry an increased risk of infection.[16] Upper respiratory tract infections are commonly reported with Jaktinib.[63] In the myelofibrosis trials, infectious pneumonia emerged as a notable Grade ≥3 adverse event, with an incidence of 10.6% in the 100 mg BID group in one long-term study and 17.8% in the ruxolitinib-intolerant population.[23]
• Other Events: In myelofibrosis trials, other common non-hematological TEAEs included elevated bilirubin, fever, and diarrhea.[40]

JAK Inhibitor Class-Specific Risks and Black Box Warnings

The entire class of oral JAK inhibitors approved for chronic inflammatory conditions is subject to a black box warning issued by the U.S. Food and Drug Administration (FDA). This warning was mandated following a large post-marketing safety study of tofacitinib, which revealed an increased risk of serious adverse events compared to TNF inhibitors.[65] The specific risks highlighted in the warning include:

• Major Adverse Cardiovascular Events (MACE), such as heart attack and stroke.
• Malignancy, including lymphoma and lung cancer.
• Thrombosis, including deep vein thrombosis (DVT) and pulmonary embolism (PE).
• All-cause mortality.

While Jaktinib will be evaluated in the context of these class-wide risks, the data from its clinical program to date have been reassuring. Notably, in the 16-week, placebo-controlled Phase II trial in axial spondyloarthritis, no events of MACE, malignancy, or thromboembolism were reported in any treatment arm.[3] Although this short-term data is encouraging, long-term surveillance will be essential to fully characterize Jaktinib's risk profile in relation to these serious class-wide concerns.

Dosage, Administration, and Regulatory Status

Dosing Regimens Investigated in Clinical Trials

The optimal dosing for Jaktinib has been systematically evaluated across its clinical programs for various indications, leading to the identification of effective and well-tolerated regimens.

• Myelofibrosis: The Phase II ZGJAK002 trial was instrumental in dose selection, comparing a 100 mg twice-daily (BID) regimen against a 200 mg once-daily (QD) regimen. The 100 mg BID dose was determined to offer a superior balance of efficacy and safety and was subsequently adopted for all pivotal Phase III studies and second-line trials in this indication.[23]
• Axial Spondyloarthritis: The Phase II trial evaluated two doses, 75 mg BID and 100 mg BID. While both were effective, the 100 mg BID dose demonstrated a trend towards greater efficacy, suggesting it may be the preferred dose for Phase III development.[3]
• Atopic Dermatitis: The ongoing Phase III program for oral Jaktinib is investigating both 75 mg BID and 100 mg BID doses.[54] The topical program has explored cream formulations with concentrations of 0.5%, 1.5%, and 2.5%.[70]

Regulatory History, Approvals, and Designations

Jaktinib, developed by Suzhou Zelgen Biopharmaceuticals Co., Ltd., has achieved significant regulatory milestones, particularly in China.[2]

• United States: On December 14, 2020, Jaktinib was granted Orphan Drug Designation by the U.S. Food and Drug Administration (FDA) for the treatment of myelofibrosis.[71] This designation provides developmental incentives but does not signify marketing approval. Jaktinib remains an investigational drug in the U.S.
• China: In a landmark achievement for the developer, Jaktinib Hydrochloride tablets were approved by China's National Medical Products Administration (NMPA) on or around May 29, 2025.[3] The approval is for the treatment of intermediate- or high-risk myelofibrosis, specifically covering primary myelofibrosis, post-polycythemia vera myelofibrosis, and post-essential thrombocythemia myelofibrosis.[3]
• Current Global Status: Jaktinib is commercially available for myelofibrosis in China. A regulatory application (NDA/BLA) has also been submitted to the NMPA for alopecia areata, placing it under review for a second major indication.[3] Globally, the drug's development is active, with multiple Phase III trials ongoing for other indications, primarily concentrated in China.[2]

Table 4: Jaktinib Regulatory Milestones and Current Status

Date	Regulatory Body	Action/Decision	Indication	Status	Source(s)
Dec 14, 2020	U.S. FDA	Orphan Drug Designation Granted	Myelofibrosis	Designated	71
May 2025	China NMPA	Marketing Approval Granted	Myelofibrosis	Approved	3
Current	China NMPA	NDA/BLA Submitted	Alopecia Areata	Under Review	3
Current	U.S. FDA	-	All indications	Investigational	71

Strategic Analysis and Future Outlook

Competitive Landscape and Positioning

Jaktinib is entering a dynamic and competitive therapeutic landscape. Its strategic positioning varies significantly by indication.

• In Myelofibrosis: The market includes several established JAK inhibitors, namely ruxolitinib, fedratinib, pacritinib, and its own parent compound, momelotinib.[3] Jaktinib's primary competitive advantage lies in its differentiated mechanism. The dual inhibition of JAK2 and ACVR1 allows it to address the "triple challenge" of myelofibrosis: splenomegaly, constitutional symptoms, and anemia. This profile positions it favorably against ruxolitinib, which can induce or worsen anemia, and makes it a direct competitor to momelotinib, which shares the ACVR1-inhibiting mechanism. The deuteration of Jaktinib may confer a pharmacokinetic advantage over momelotinib, potentially leading to more stable drug exposure and an optimized dosing schedule. Furthermore, its demonstrated superiority in both efficacy and hematologic safety over hydroxyurea in the front-line setting provides a strong rationale for its use as a first-line agent, particularly in patients presenting with anemia or cytopenias.[25]
• In Inflammatory Diseases: For indications like atopic dermatitis, alopecia areata, and ankylosing spondylitis, Jaktinib will compete in crowded and high-value markets. These fields are dominated by a range of biologics (e.g., TNF inhibitors, IL-17 inhibitors, IL-4/13 inhibitors) and other highly effective oral JAK inhibitors (e.g., tofacitinib, baricitinib, upadacitinib).[4] Success in these areas will be contingent upon demonstrating a superior or clearly differentiated efficacy and safety profile in pivotal head-to-head clinical trials against established standards of care.

Unmet Needs and Future Development Trajectory

Jaktinib's development program is well-aligned with significant unmet clinical needs.

• Myelofibrosis: It directly addresses the need for a single agent that can comprehensively manage all major facets of the disease, especially the challenging issue of anemia. It also provides a crucial new option for the growing population of patients who fail or become intolerant to ruxolitinib, for whom outcomes are historically poor.
• Future Trajectory: The aggressive pursuit of Phase III programs in dermatology (AA, AD) and rheumatology (axSpA) signals a clear corporate strategy to expand Jaktinib's footprint beyond hematology into larger primary care and specialty markets. Future avenues of development will likely include combination therapies, such as with azacitidine for myelodysplastic syndromes with myelofibrosis (as suggested by trial NCT04866056), to further enhance efficacy.[2] Expansion into pediatric populations and the initiation of head-to-head trials against other JAK inhibitors will be critical steps to establish superiority and define its ultimate place in therapy.

Concluding Remarks and Expert Recommendations

Jaktinib is a strategically designed, second-generation JAK inhibitor characterized by a compelling and differentiated clinical profile. Its dual inhibition of JAK2 and ACVR1 provides a unique therapeutic advantage in myelofibrosis, which has been validated by its recent marketing approval in China based on robust Phase III data. This approval marks a major milestone for the compound and its developer.

The future success of Jaktinib will depend on several key factors. In myelofibrosis, the key will be to translate its unique anemia-mitigating mechanism into a clear clinical advantage that drives adoption in the global marketplace. For its inflammatory indications, navigating the highly competitive landscape will require robust data from ongoing Phase III trials, ideally including head-to-head comparisons to define its relative value. Finally, as with all drugs in its class, the accumulation of long-term safety data will be crucial for addressing the class-wide black box warning concerns and ensuring physician and patient confidence.

It is recommended that stakeholders closely monitor the readouts from the ongoing Phase III trials in atopic dermatitis and ankylosing spondylitis, as these will be pivotal in shaping the drug's future. The long-term safety and survival data from the myelofibrosis extension studies will also be critical for solidifying its position as a foundational therapy for this disease.

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