Abstract
Golidocitinib (高瑞哲®) is an oral, potent, selective Janus kinase 1 (JAK1) inhibitor being developed by Dizal (Jiangsu) Pharmaceutical Co., Ltd for the treatment of cancer, including peripheral T cell lymphoma (PTCL). In June 2024, golidocitinib received conditional approval in China for the treatment of adult patients with relapsed or refractory (r/r) PTCL who have received at least one line of systemic treatment. This article summarizes the milestones in the development of golidocitinib leading to this first approval for the treatment of adults with PTCL.
Avoid common mistakes on your manuscript.
Digital Features for this AdisInsight Report can be found at https://doi.org/10.6084/m9.figshare.26860279. |
An oral, potent, selective JAK1 inhibitor being developed by Dizal for the treatment of cancer, including PTCL |
Received its first approval (conditional approval) on 18 June 2024 in China |
Approved for the treatment of adult patients with r/r PTCL who have received at least one line of systemic treatment |
1 Introduction
Peripheral T cell lymphomas (PTCL) are rare, aggressive, heterogeneous group of non-Hodgkin lymphoma (NHL) that has multiple subtypes. PTCL accounts for 5–10% of NHL in Western countries, and 12-22% of NHL in Asian countries [1]. Relapse after initial treatment [most commonly CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisolone)-based induction therapy followed by consolidation autologous haematopoietic stem cell transplant (HSCT)] is frequent [1]. The prognosis in patients with relapsed or refractory (r/r) PTCL is poor, with a 3-year overall survival (OS) rate of < 30% [2]; thus, there is an unmet need for better therapies in patients with r/r PTCL [3]. The Janus-associated kinase (JAK) family kinases are strongly associated with cancer, and dysregulation of JAK/STAT signaling (especially increased activation of STAT3) is associated with multiple malignancies [1, 4]. The JAK/STAT pathway is implicated in the pathogenesis of PTCL, making it a promising target [5]. JAK1 is the primary driver of STAT3 phosphorylation and signalling, while JAK2 is essential for signal transduction downstream of erythropoietin, thrombopoietin, and other related receptors that control erythrocyte and megakaryocyte expansion [4, 6]. JAK2 inhibition is thought to be associated with haematological toxicities [4, 6]; consequently, drugs that preferentially target JAK1 may achieve good efficacy with fewer toxicities [4].
Golidocitinib (高瑞哲®), an oral, potent, selective JAK1 inhibitor that has shown promising antitumour activity in vitro and in vivo [4, 7, 8], is being developed by Dizal (Jiangsu) Pharmaceutical Co., Ltd for use in the treatment of cancer, including PTCL [9]. In June 2024, golidocitinib was conditionally approved in China for the treatment of adult patients with r/r PTCL who have received at least one line of systemic treatment [8, 10]. Approval was granted on the basis of the overall response rate (ORR) and duration of response (DoR) from a single arm clinical trial; routine approval of this indication will depend on results of subsequent confirmatory randomized, controlled clinical trials [8]. The recommended dose of golidocitinib is 150 mg once daily, with or without food, until disease progression or intolerable adverse reactions occur. During golidocitinib treatment, prevention of Pneumocystis jiroveci pneumonia (PJP) should be considered, and preventive and monitoring measures should be taken in patients with high risk factors for herpes virus reactivation. Golidocitinib is contraindicated in pregnant and lactating women [8]. Warnings and precautions relating to golidocitinib treatment include the risk of serious infections, such as infectious pneumonia, viral infection and reactivation [herpes virus and hepatitis B virus (HBV)], and PJP. Patients should be closely monitored for changes in infection symptoms and signs during treatment. Golidocitinib treatment interruption or permanent discontinuation may be necessary for grade 3 or 4 decreased platelet counts, other grade 4 haematological adverse reactions, febrile neutropenia and grade 3 herpes zoster. Treatment with golidocitinib should be permanently discontinued if HBV reactivation, ocular complications of herpes virus reactivation, drug-induced lung injury or grade ≥ 3 non-haematological adverse reactions occur [8].
Coadministration of golidocitinib with strong CYP3A inhibitors may increase the exposure of golidocitinib and should be avoided; coadministration with moderate CYP3A inhibitors should be avoided unless the benefits outweigh the risks and treatment with a CYP3A inhibitor is necessary. Coadministration of golidocitinib with strong or moderate inducers of CYP3A may reduce exposure to golidocitinib and coadministration with strong CYP3A inducers should be avoided. Golidocitinib inhibits the renal transporters MATE1 and MATE2-K, increasing exposure of MATE1 and MATE2-K substrate drugs at clinical therapeutic doses. MATE1 and MATE2-K substrate drugs with narrow therapeutic windows should be used with caution during golidocitinib treatment [8].
Dosage adjustments are not required in patients with mild hepatic impairment [total bilirubin ≤ upper limit of normal (ULN)] and AST > ULN or total bilirubin > 1–1.5 × ULN with any AST level] or mild to moderate renal impairment [creatinine clearance (CLCR ≥ 30 mL/min]. However, the safety and efficacy of golidocitinib in patients with moderate (total bilirubin > 1.5–3.0 × ULN with any AST level) or severe (total bilirubin > 3.0 × ULN with any AST level) hepatic impairment, or with severe renal insufficiency (CLCR < 30 mL/min) or requiring dialysis, has not been established [8].
1.1 Company Agreements
In November 2017, AstraZeneca entered into a strategic joint venture with the Chinese Future Industry Investment Fund to form Dizal, an equally-owned, stand-alone company in China, to discover, develop and commercialize new therapeutic drugs [11].
2 Scientific Summary
2.1 Pharmacodynamics
In biochemical assays, golidocitinib potently and selectively inhibited the enzymatic activity of JAK1 (IC50 0.07 µM), and showed > 214-fold selectivity for JAK1 over JAK2 (IC50 > 15 µM), inhibition of pSTAT3 in NCI-H19785 cells (IC50 0.130) and negligible hERG activity (> 100 µM). Golidocitinib was inactive towards JAK3 (IC50 > 30 µM) and showed moderate activity towards TYK2 (IC50 2.8 µM) [4]. In T-cell lymphoma cell lines with abnormal expression of the JAK/STAT pathway and mouse T-cell lymphoma xenograft models, golidocitinib inhibited STAT3 phosphorylation signaling, induced apoptosis, and inhibited tumour cell proliferation and tumour growth [7, 8, 12]. In mouse T-cell lymphoma xenograft models, golidocitinib administration was associated with hepatic impairment and dyslipidemia; subsequent transcriptome sequencing analysis found that golidocitinib upregulated expression of mTOR pathway‐related genes. The combination of golidocitinib with the mTOR inhibitor everolimus showed synergistic anti‐PTCL efficacy in vitro and in vivo, and significantly reduced golidocitinib‐induced mTOR-related adverse effects [12]. In a mouse xenograft model of T790M EGFR mutant non-small cell lung cancer (NSCLC), golidocitinib inhibited STAT3 phosphorylation signaling, and when coadministered with osimertinib, enhanced the antitumour activity of osimertinib [8]. In patients with r/r PTCL who were treated with golidocitinib 150 mg once daily, the inhibition rate of cytokine-induced STAT3 phosphorylation in whole blood at steady state was ≈ 58%, indicating that golidocitinib can continuously inhibit the JAK/STAT signaling pathway during the administration period [8].
At clinically relevant exposures, golidocitinib had no clinically significant effect on the QT interval [8].
2.2 Pharmacokinetics
The systemic exposure of oral golidocitinib (Cmax and AUC) was approximately dose proportional in patients with r/r PTCL (dose range 150–250 mg) and in healthy volunteers (dose range 5–150 mg) [8, 13]. Median Tmax was 2–4 h after a single dose of golidocitinib 150 mg in patients with r/r PTCL and in healthy subjects [8]. Steady-state plasma concentrations of were achieved within 15 days following administration of golidocitinib 150 mg once daily in patients with r/r PTCL; accumulation ratios for Cmax and AUC were 2.4 and 3.4, respectively, and the steady state peak-to-trough concentration ratio was ≈ 2-fold [8]. Food had no significant effect on golidocitinib systemic exposure in patients with r/r PTCL or healthy subjects [8, 13]. Golidocitinib is ≈ 63% bound to human plasma proteins in vitro. The whole blood-to-plasma concentration ratio of golidocitinib is 1.276 and apparent Vd after administration of golidocitinib 150 mg in healthy subjects is 1213–1400 L [8]. Golidocitinib is metabolized in the liver, primarily by CYP3A4 and CYP3A5 (based on in vitro studies); in a body mass balance study, unchanged golidocitinib accounted for 58% of total radioactivity in plasma. In healthy subjects, CL/F after a single oral dose of golidocitinib was 18.1–21.9 L/h and t1/2 was 46.3–47.5 h. After a single oral dose of radiolabeled golidocitinib in healthy subjects, 37% of the dose was excreted in faeces (as metabolites; no unchanged drug detected) and 45% was excreted in urine (≈ 29% as the unchanged drug) [8]. Based on a population PK analysis, mild hepatic impairment and mild or moderate renal impairment had no clinically relevant effect on golidocitinib pharmacokinetic parameters. The pharmacokinetics of golidocitinib in patients with moderate or severe hepatic impairment has not been established [8].
Coadministration of golidocitinib with itraconazole (a potent CYP3A inhibitor) increased golidocitinib Cmax by 8.3% and AUC∞ by 50.6%. Coadministration of golidocitinib with carbamazepine (a potent CYP3A inducer) reduced golidocitinib Cmax by 28.1% and AUC∞ by 50.5%. Based on physiological PK modelling, coadministration of a moderate CYP3A inhibitor (erythromycin or fluconazole) with golidocitinib is predicted to increase golidocitinib Cmax,ss (by 30 and 48%, respectively) and AUCss (by 40 and 58%). Steady-state exposure of golidocitinib was not significantly increased when coadministered with a weak CYP3A4 inhibitor (cimetidine). Based on physiological PK modelling, coadministration of golidocitinib with a moderate CYP3A4 inducer (efavirenz) is predicted to reduce golidocitinib Cmax,ss by 43% and AUCss by 51% [8].
Although at clinical doses golidocitinib is a reversible inhibitor of CYP3A4, physiological PK modelling predicted that exposure of CYP3A4 sensitive substrates (e.g., simvastatin and midazolam) would be unchanged when coadministered with golidocitinib. Golidocitinib does not show clinically relevant reversible or time-dependent inhibition of other major CYP enzyme subtypes. Golidocitinib is a weak inducer of CYP1A2 and 2B6, but has no clinically relevant induction effect on CYP3A4, CYP2C8, CYP2C9 and CYP2C19 [8].
Golidocitinib is a substrate for P-gp, but not for BCRP, OATP1B1, and OATP1B3. At clinical doses, golidocitinib is an inhibitor of MATE1 and MATE2-K and may inhibit BCRP; however, physiological PK modelling predicted that exposure of BCRP substrates (e.g., rosuvastatin) would be unchanged when coadministered with golidocitinib. Golidocitinib is not an inhibitor of P-gp, OAT1, OAT3, OATP1B1, OATP1B3, and OCT2 [8].
Features and properties of golidocitinib
Alternative names | 高瑞哲®; DZD4205; AZD4205 |
Class | Acetamides; Anti-inflammatories; Antineoplastics; Indoles; Piperazines; Pyrazoles; Pyrimidines; Small molecules |
Mechanism of action | Janus kinase 1 inhibitors |
Route of administration | Oral |
Pharmacodynamics | > 214-fold selectivity for JAK1 over JAK2 (IC50 0.07 vs > 15 µM), potent inhibition of pSTAT3 in NCI-H19785 cells (IC50 0.130), negligible hERG activity (> 100 µM) Inhibited STAT3 phosphorylation signaling, induced apoptosis, inhibited tumour cell proliferation and tumour growth in T-cell lymphoma cell lines with abnormal expression of the JAK/STAT pathway, and in mouse T-cell lymphoma and T790M EGFR mutant NSCLC xenograft models |
Pharmacokinetics | Median Tmax 2–4 h; steady state peak-to-trough concentration ratio ≈ 2-fold; ≈ 63% human plasma protein bound; apparent Vd 1213–1400 L; CL/F 18.1–21.9 L/h; t1/2 46.3–47.5 h; 37% of a dose excreted in faeces and 45% excreted in urine |
Adverse events | |
Most frequent (incidence > 10%) | Neutropenia, thrombocytopenia, leukopenia, anemia, lymphocytopenia, increased AST, increased ALT, hypofibrinogenemia, increased blood CPK, hypercholesterolemia, hypertriglyceridemia, increased serum creatinine, infectious pneumonia (including 2 cases of PJP) |
Other clinically significant adverse events (incidence < 10%) | Herpes zoster, urinary tract infection, upper respiratory tract infection, HBV reactivation, CMV infection reactivation, herpes simplex (2.2%) |
Rare | Pneumocystis jiroveci pneumonia (2 cases) |
ATC codes | |
WHO ATC code | A07E (Intestinal Anti-inflammatory Agents) |
EphMRA ATC code | L01X-E (Protein kinase inhibitors) |
Chemical name | (2R)-N-[3-[2-[(3-methoxy-1-methylpyrazol-4-yl)amino]pyrimidin-4-yl]-1H-indol-7-yl]-2-(4-methylpiperazin-1-yl)propanamide |
2.3 Therapeutic Trials
Golidocitinib showed promising anti-tumour activity in the single-arm, multinational, phase 2 JACKPOT8 Part B (NCT04105010) trial in patients with r/r PTCL who had received at least one prior systemic therapy [14]. At a median follow-up of 13.3 months, treatment with golidocitinib 150 mg once daily resulted in an Independent Review Committee (IRC)-assessed ORR of 44.3% (primary endpoint)] and a combined complete response rate (CRR) of 23.9% in the activity analysis set (n = 88). The median time to first documented response was 1.4 months. In the subgroup of patients with data on change in target lesion size (n = 70), 49 (70%) had a reduction in tumour size. IRC-assessed median DoR was 20·7 months (median follow-up 12·5 months) and median progression-free survival (PFS) was 5·6 months (median follow-up 11·9 months) [14]. At baseline, 94% of patients were Asian and 73% had received ≥ 2 lines of prior systemic therapies. Golidocitinib was administered until disease progression, unacceptable toxicity, death or other discontinuation criteria were met. Prophylaxis for PJP was mandatory for all patients. Patients had to have at least one measurable lesion, and ORR was assessed based on CT scans per Lugano 2014 criteria. A complete CRR consisted of a complete radiological response confirmed with post-treatment bone marrow biopsy [14].
In the earlier phase 1 JACKPOT8 Part A (NCT04105010) dose-escalation trial, golidocitinib had showed promising anti-tumour activity in heavily pretreated patients with r/r PTCL [7]. In golidocitinib 150 mg once daily recipients (n = 35) ORR was 40% and CRR was 25.7%, and in golidocitinib 250 mg once daily recipients (n = 16) ORR was 37.5% and CRR was 12.5%. In the overall population (n = 51), median DoR was 8.0 months (median follow-up 14.7 months) and median PFS was 3.3 months (median follow-up 15.9 months). All enrolled patients were Asian; at baseline, patients had undergone a median 2 lines of prior systemic therapies and 41.2% had received ≥ 3 lines [7].
Golidocitinib 150 mg once daily showed promise in maintaining tumour response after first-line systemic therapy in patients with PTCL in the phase 2 JACKPOT26 (NCT06511869) trial [15]. In the cohort of patients with a complete response (CR) post first-line therapy (Cohort 1; n = 30), median disease-free survival (DFS) had not been reached at a median 12 month’s follow-up and 76.7% of patients remained event free. In the cohort of patients with a partial response (PR) post first-line therapy (Cohort 2; n = 18), ORR was 38.9% and CRR was 33.3%; median DoR had not been reached. Median PFS was 16.7 months at a median 10 months’ follow-up and 61.1% patients remained event free [15]. JACKPOT26 enrolled patients with PTCL who had achieved tumour response (CR or PR) with first-line therapy but were ineligible for HSCT or HSCT was not planned. Patients received golidocitinib for a maximum of 13 28-day cycles or until discontinuation criteria were met. Most patients (73%) had received CHOP-based first-line therapy [15].
Key clinical trials of golidocitinib
Drug(s) | Indication | Phase | Status | Location(s) | Sponsor/collaborator | Identifier |
---|---|---|---|---|---|---|
Golidocitinib | r/r PTCL | 1/2 | Completed | China, USA, Australia | Dizal | NCT04105010; JACKPOT8 |
Golidocitinib | r/r PTCL | 2 | Recruiting | China | Dizal | NCT06511895; JACKPOT27 |
Golidocitinib, CHOP regimen | PTCL | 2 | Recruiting | China | Henan Cancer Hospital | NCT05963347 |
Golidocitinib | PTCL | 2 | Ongoing | China | Dizal | NCT06511869; JACKPOT26 |
Golidocitinib, sintilimab, platinum doublet chemotherapy | PD-L1+ NSCLC | 2 | Not yet recruiting | China | Cancer Institute and Hospital; Chinese Academy of Medical Sciences; Dizal | NCT06198907; JACKPOT33 |
Golidocitinib, sunvozertinib | EGFR mutant NSCLC | 2 | Recruiting | China | Dizal | NCT06295432; WU-KONG21 |
Golidocitinib, osimertinib | EGFR mutant NSCLC | 1/2 | Completed | Australia | Dizal | NCT03450330; JACKPOT1 |
2.4 Adverse Events
The most common adverse events (incidence ≥ 10%) reported in patients treated with golidocitinib in five clinical trials (n = 274; includes 179 patients with r/r PTCL who were administered golidocitinib 150 mg once daily) [8] were neutropenia [56.6% (all grades); 29.6% (grade ≥ 3)], thrombocytopenia (54.0%; 11.7%), leukopenia (52.9%; 20.4%), anemia (29.9%; 5.8%), lymphocytopenia (28.1%; 13.5%), increased AST (25.9%; 2.2%), increased ALT (20.8%; 1.5%), hypofibrinogenemia (14.6% vs 1.5%), increased blood CPK (14.6%; 1.1%), hypercholesterolemia (14.6%; 0.0%), hypertriglyceridemia (14.2%; 1.8%), increased serum creatinine (12.4%; 0.4%) and infectious pneumonia (including two cases of PJP) [11.7%; 5.5%,]; one case resulted in death. Other clinically significant adverse reactions (incidence < 10%) included included herpes zoster (7.7%), urinary tract infection (6.9%), upper respiratory tract infection (6.2%), HBV reactivation (4.0%), cytomegalovirus infection reactivation (2.6%), and herpes simplex (2.2%) [8]. 61 of 274 patients (22.3%) had serious adverse reactions; the most frequent (incidence ≥ 2%) were infectious pneumonia (5.8%), herpes zoster (2.6%) and thrombocytopenia (2.6%). Infections, serious infections and ≥ grade 3 infections occurred in 30.7%, 11.3 and 13.1% of golidocitinib recipients, respectively. 2 of 274 patients treated with golidocitinib had fatal adverse reactions (1 case each of infectious pneumonia and liver failure). 37.2% of golidocitinib recipients had treatment suspension due to adverse reactions, 9.5% had dose reductions due to adverse reactions and 7.3% discontinued treatment because of adverse reactions. The most common adverse reactions leading to discontinuation of treatment, dose reduction or suspension of administration were infectious pneumonia, interstitial lung disease, neutropenia, thrombocytopenia, and herpes zoster [8]. The adverse events profile of golidocitinib in patients with r/r PTCL in the JACKPOT8 Part B [14], JACKPOT8 Part A [7] and JACKPOT26 [15] trials was consistent with that in the pooled population.
2.5 Ongoing Clinical Trials
Several golidocitinib trials are ongoing in China, including a phase 2 monotherapy trial in r/r PTCL (JACKPOT27; NCT06511895); a phase 2 trial of golidocitinib maintenance therapy in PTCL after completion of standard first-line therapy (JACKPOT26; NCT06511869); an investigator-led phase 2 trial in combination with CHOP as frontline treatment for PTCL (NCT05963347); and a phase 2 trial in combination with sunvozertinib in standard-treatment-failed EGFR mutant advanced NSCLC (WU-KONG21; NCT06295432). A phase 2 trial of golidocitinib in combination with sintilimab as front-line treatment in metastatic PD-L1+ NSCLC (JACKPOT33; NCT06198907) will commence recruiting shortly.
3 Current Status
Golidocitinib received its first approval on 18 June 2024 for the treatment of adult patients with r/r PTCL who have received at least one line of systemic treatment in China. [8, 10]. This approval is conditional and was granted based on ORR and DoR results from a single arm clinical trial; routine approval of this indication will depend on results of subsequent confirmatory randomized, controlled clinical trials [8]. A randomised, controlled trial is being planned to assess the efficacy and confirm the activity of golidocitinib [14].
References
Chang EWY, Tan YH, Chan JY. Novel clinical risk stratification and treatment strategies in relapsed/refractory peripheral T-cell lymphoma. J Hematol Oncol. 2024. https://doi.org/10.1186/s13045-024-01560-7.
Bellei M, Foss FM, Shustov AR, et al. The outcome of peripheral T-cell lymphoma patients failing first-line therapy: a report from the prospective, International T-Cell Project. Haematologica. 2018;103(7):1191–7.
Huang H, Zhang W, Deng X, et al. Novel agents and regimens in relapsed or refractory peripheral T-cell lymphoma: latest updates from 2023 ASH annual meeting. Exp Hematol Oncol. 2024. https://doi.org/10.1186/s40164-024-00510-w.
Su Q, Banks E, Bebernitz G, et al. Discovery of (2R)-N-[3-[2-[(3-Methoxy-1-methyl-pyrazol-4-yl)amino]pyrimidin-4-yl]-1H-indol-7-yl]-2-(4-methylpiperazin-1-yl)propenamide (AZD4205) as a potent and selective Janus kinase 1 inhibitor. J Med Chem. 2020;63(9):4517–27.
Moskowitz AJ, Ghione P, Jacobsen E, et al. A phase 2 biomarker-driven study of ruxolitinib demonstrates effectiveness of JAK/STAT targeting in T-cell lymphomas. Blood. 2021;138(26):2828–37.
Brooks AJ, Putoczki T. JAK-STAT signalling pathway in cancer. Cancers (Basel). 2020. https://doi.org/10.3390/cancers12071971.
Song Y, Yoon DH, Yang H, et al. Phase I dose escalation and expansion study of golidocitinib, a highly selective JAK1 inhibitor, in relapsed or refractory peripheral T-cell lymphomas. Ann Oncol. 2023;34(11):1055–63.
Dizal (Jiangsu) Pharmaceutical Co Ltd. Golidocitinib: Chinese prescribing information. Shanghai: Dizal (Jiangsu) Pharmaceutical Co Ltd; 2024.
Dizal (Jiangsu) Pharmaceutical Co Ltd. Pipeline and strategy. 2023. https://dizalpharma.com/innovation/P&S. Accessed 12 Aug 2024.
Dizal (Jiangsu) Pharmaceutical Co Ltd. Golidocitinib approved in China as first-in-class JAK1 only inhibitor for the treatment of relapsed or refractory peripheral T-cell lymphoma [media release]. 19 June 2024. https://www.dizalpharma.com/.
AstraZeneca. AstraZeneca and Chinese Future Industry Investment Fund establish joint venture to develop new medicines in China [media release]. 27 Nov 2017. https://www.astrazeneca.com.
Ye Y, Wu M, Mi L, et al. The mTOR kinase inhibitor everolimus synergistically enhances the anti-tumor effect of the Janus kinase 1 (JAK1) inhibitor AZD4205 on Peripheral T cell lymphoma [abstract no. 418]. Hematol Oncol. 2023;41(S2):558–9.
Chen K, Guan X, Yang Z, et al. Pharmacokinetic characteristics of golidocitinib, a highly selective JAK1 inhibitor, in healthy adult participants. Front Immunol. 2023. https://doi.org/10.3389/fimmu.2023.1127935.
Song Y, Malpica L, Cai Q, et al. Golidocitinib, a selective JAK1 tyrosine-kinase inhibitor, in patients with refractory or relapsed peripheral T-cell lymphoma (JACKPOT8 Part B): a single-arm, multinational, phase 2 study. Lancet Oncol. 2024;25(1):117–25.
Jin J, Cai QQ, Zhang LL, et al. Phase 2 study of golidocitinib, a JAK1 selective inhibitor, as maintenance therapy in patients with peripheral T cell lymphomas after first-line systemic therapy (JACKPOT26) [abstract no. 4430 plus poster]. Blood. 2023;142(Suppl 1):4430–2.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Funding
The preparation of this review was not supported by any external funding.
Authorship and Conflict of interest
During the peer review process the manufacturer of the agent under review was offered an opportunity to comment on the article. Changes resulting from any comments received were made by the authors on the basis of scientific completeness and accuracy. Susan J. Keam is a contracted employee of Adis International Ltd/Springer Nature, and declares no relevant conflicts of interest. All authors contributed to this article and are responsible for its content.
Ethics approval, Consent to participate, Consent to publish, Availability of data and material, Code availability
Not applicable.
Additional information
This profile has been extracted and modified from the AdisInsight database. AdisInsight tracks drug development worldwide through the entire development process, from discovery, through pre-clinical and clinical studies to market launch and beyond.
Supplementary Information
Rights and permissions
Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
About this article
Cite this article
Keam, S.J. Golidocitinib: First Approval. Drugs (2024). https://doi.org/10.1007/s40265-024-02089-2
Accepted:
Published:
DOI: https://doi.org/10.1007/s40265-024-02089-2