Optimizing Pharmacotherapy In Chronic GVHD

Originally published by our sister publication Specialty Pharmacy Continuum

Chronic graft-versus-host disease (cGVHD) can occur in a multitude of organs, often characterized by fibrosis or autoimmune-like syndromes. This article reviews the prevalence, diagnosis, and treatment options for cGVHD, including recent drug approvals and latest guidelines, and highlights the role pharmacists can play in the management of this post–hematopoietic stem cell transplantation (post-HCT) complication.

GVHD, an immunologic disorder affecting multiple organ systems, occurs when transplanted stem cells or bone marrow (the graft) recognize the recipient’s healthy tissues (the host) as foreign and launch an immune attack. This reaction can also happen after an organ transplant.¹

GVHD is a leading cause of morbidity and non-relapse mortality with a significant impact on quality of life.² This immunologic disorder can be either acute or chronic, based on timing and clinical presentation.^2-4

Acute GVHD (aGVHD) is caused by an allogeneic inflammatory response that can involve 3 organs: the liver (hyperbilirubinemia), skin (inflammatory maculopapular erythematous skin rash), and the gastrointestinal tract (large volume of watery diarrhea, abdominal cramping).³ Chronic GVHD was defined originally as any GVHD presentation beyond 100 days, but now is defined based on organ severity and specific diagnostic signs accompanied by confirmation (eg, tissue biopsy) in at least 1 target organ demonstrating hallmark changes on hematopathology review.

Prevalence

Typically, cGVHD arises in about 30% to 50% of all allogeneic HCT patients who receive standard GVHD prophylaxis.⁵ The Center for International Blood and Marrow Transplant Research and U.S. claims analysis data have shown an increase in overall cGVHD incidence, likely related to the increasing number of HCTs performed each year and prolonged survival of patients after HCT.^4,6 Risk factors for cGVHD include matched and mismatched unrelated donor and haploidentical transplants, use of peripheral blood versus bone marrow stem cells, older recipient age, female-to-male transplantation, myeloablative versus reduced-intensity preparative chemotherapy, and a history of aGVHD.^6-9

Diagnosis and Scoring

Chronic GVHD is complex, and the pathophysiology is mainly characterized by impaired mechanisms that affect adaptive and innate immunity.⁸ Chronic GVHD can occur at any point after allogeneic HCT, but typically occurs more than 100 days after transplant. The National Institutes of Health developed a framework for diagnosing and grading cGVHD, which is used as a standard in clinical trials and practice.¹⁰ Two subcategories of cGVHD exist:

1. classic cGVHD without features of aGVHD; and
2. an overlap syndrome, which refers to the presence of at least 1 aGVHD manifestation in a patient with cGVHD.

Chronic GVHD is diagnosed based on the symptoms involving organs/organ systems (eg, the skin, eyes, oral mucosa, liver, gastrointestinal tract, genitalia, lungs, and musculoskeletal system), laboratory values, and pulmonary function tests.^10,11 There also is a classification system based on organ-specific grading; the overall severity of cGVHD is calculated using this organ-specific grading and the number of organs affected.³

Prevention and Treatment

The cornerstone of GVHD prevention includes optimal donor selection and pharmacologic support (combination immunosuppressant therapy with/without antithymocyte globulin or post-transplant cyclophosphamide if using haploidentical donors).¹² Despite these preventive measures, cGVHD occurs in up to half of patients undergoing HCT. Goals for the treatment of cGVHD include a sustained reduction or elimination of symptom burden, disability, and disease progression. Clinicians must weigh the risks versus benefits of treatment regimens, and tailor therapy based on each patient’s presentation and comorbidities. Of note, a shift in treatment from broad immunosuppression to biologically targeted therapies has been observed in recent years.¹³

The European Society for Blood and Marrow Transplantation (EBMT) published consensus recommendations on the prophylaxis and management of GVHD in adults after allogeneic HCT, which were updated in 2024.¹⁴ The National Comprehensive Cancer Network (NCCN) also released a guideline for the management of GVHD after HCT in 2025.¹⁵ The decision to start treatment for cGVHD is based on various factors such as symptom type, severity, and dynamics of disease progression.^14,15 Table 1 details first-line treatment regimens for cGVHD, which are outlined in the EBMT and NCCN guidelines, respectively.

Table 1. Guideline Comparison on the Treatment of cGVHD
Guideline	First-line therapy	Additional therapy
NCCN 2025	Clinical trial or Continue or consider restarting original immunosuppressive agent and/or Systemic corticosteroids: 0.5-1 mg/kg/d methylprednisolone (or prednisone dose equivalent) or Sirolimus + prednisone with/without Topical steroids as clinically indicateda and/or Inhaled steroids with + azithromycin + montelukast for lung involvement (eg, FAM)	If there is a response, taper steroids as clinically feasible to reduce long-term steroid side effects and risk for infection.
		If no response (steroid-refractory disease), consider a clinical trial or addition of systemic agent to corticosteroids, with steroid taper as clinically feasible. FDA-approved systemic agents include ibrutinib, ruxolitinib, belumosudil, and axatilimab-csfr.
EBMT 2024	Systemic corticosteroids (first choice being oral prednisone at a dosage of 1 mg/kg/d)b or If already receiving corticosteroid treatment, the dose of corticosteroid can be increased (if it is <1 mg/kg), and an alternate strategy is usually applied (ie, CNI or extracorporeal photopheresis) or If already receiving full-dose corticosteroid and cyclosporine A at the time of cGVHD onset, continue corticosteroid and cyclosporine A with optimal supportive measures; can also change immunosuppressive therapy; treat these patients in clinical trials, if possible with/without FAM regimen in combination with systemic steroids for initial treatment of bronchiolitis obliterans syndrome	In severe cGVHD cases, addition of another immunosuppressant to reduce steroid use is an option. There is no standard second-line treatment for cGVHD.c
		In steroid-refractory disease, the EBMT recommends ruxolitinib. Other potential therapeutic options include belumosudil and ibrutinib.
cGVHD, chronic graft-vs-host disease; CNI, calcineurin inhibitor; EBMT, European Society for Blood and Marrow Transplantation; FAM, fluticasone, azithromycin, montelukast; JAK, Janus kinase; mTOR, mechanistic target of rapamycin; NCCN, National Comprehensive Cancer Network; NIH, National Institutes of Health. a Topical steroids (eg, clobetasol, triamcinolone), topical estrogen (for vulvovaginal GVHD), topical tacrolimus, or dexamethasone oral rinse (for oral GVHD). Medium- to high-potency formulations are advised for most areas, except for the face and intertriginous regions, where low-potency hydrocortisone is appropriate. b Randomized trials that evaluated the addition of other agents (azathioprine, cyclosporine, hydroxychloroquine, mycophenolate mofetil, or thalidomide) to a prednisone regimen did not show a clinically significant benefit in patients with standard-risk cGVHD, according to NIH classification. c Follow institutional guidelines; common components of second-line treatment—in addition to steroids—are CNIs, extracorporeal photopheresis, ibrutinib, JAK inhibitors, mycophenolate mofetil, rituximab, mTOR inhibitors, pentostatin, proteasome inhibitors, and tyrosine kinase inhibition. Based on references 13 and 14.

Chronic GVHD can also develop into steroid-refractory disease, which may be defined as disease progression after a patient has been on a prednisone dose equivalent of at least 1 mg/kg per day for 1 to 2 weeks or has stable cGVHD disease while on at least 0.5 mg/kg per day (or 1 mg/kg every other day) of prednisone for 1 to 2 months.¹⁵ The NCCN guideline outlines systemic agents for steroid-refractory cGVHD to be used in conjunction with corticosteroids. Approximately 40% to 50% of patients with cGVHD will be steroid-refractory. There is insufficient evidence to recommend one agent over another, and selection should be based on factors including accessibility, patient tolerability, drug–drug interactions, and the effectiveness of prior treatment. The choice of agent may also be influenced by the extent of organ involvement and overall severity of cGVHD.

In recent years, the FDA has approved 4 agents for the treatment of cGVHD: ibrutinib (Imbruvica, Pharmacyclics/Janssen), ruxolitinib (Jakafi, Incyte), belumosudil (Rezurock, Kadmon), and axatilimab-csfr (Niktimvo, lncyte).^16-19 Dosing and administration considerations for these agents are summarized in Table 2 (page 17). All 4 FDA-approved cGVHD treatments work by targeting immune cells, either by inhibiting kinases involved in cytokine and growth factor signaling or reducing pro-inflammatory myeloid cells.⁵ While ibrutinib and ruxolitinib are approved for use after at least 1 prior line of systemic therapy, axatilimab-csfr and belumosudil are authorized for use only after at least 2 prior lines of therapy.

Table 2. FDA-Approved Agents for Treatment of cGVHD
Generic name (brand name, manufacturer)	Mechanism of action	Approved indications	Dosage and administration for cGVHD	Key warnings, precautions, and AEs
Axatilimab-csfr (Niktimvo, Incyte)	Monoclonal antibody that targets CSF-1R found on monocytes and macrophages. By blocking CSF-1R, it decreases pro-inflammatory and profibrotic monocytes and macrophages. This inhibition also suppresses pathogenic macrophage activity in tissues.	Treatment of cGVHD after failure of =2 prior lines of systemic therapy in adult and pediatric patients weighing =40 kg	Administered only as an IV infusion over 30 min Recommended dosage: 0.3 mg/kg (maximum, 35 mg) every 2 wk until progression or unacceptable toxicity	Warnings/precautions Infusion-related reactions Embryo-fetal toxicity Common AEs (=15%) Laboratory abnormalities Musculoskeletal pain Viral infection Fatigue Nausea Headache Diarrhea Cough Bacterial infection Pyrexia Dyspnea
Belumosudil (Rezurock, Kadmon)	ROCK inhibitor that targets ROCK2 and ROCK1 with varying potency. It has been shown to downregulate pro-inflammatory responses and suppress pro-fibrotic signaling in vitro.	Treatment of cGVHD after failure of =2 prior lines of systemic therapy in adult and pediatric patients =12 y	Recommended dosage: 200 mg taken orally once daily with food until progression of cGVHD requires new systemic therapy	Warnings/precautions Embryo-fetal toxicity Common AEs (=20%) Laboratory abnormalities Infections Asthenia Nausea Diarrhea Dyspnea Cough Edema Hemorrhage Abdominal pain Musculoskeletal pain Headache
Ibrutinib (Imbruvica, Pharmacyclics/Janssen)	Small-molecule inhibitor that binds to BTK, blocking its activity. BTK plays a key role in B-cell receptor and cytokine signaling, influencing B-cell movement, chemotaxis, and adhesion.	Adult patients with CLL/SLL Adult patients CLL/SLL with 17p deletion Adult patients with WM Adult and pediatric patients age =1 y with cGVHD after failure of 1 or more lines of systemic therapy	Patients =12 y: 420 mg taken orally once daily Patients 1 to <12 y: 240 mg/m2 taken orally once daily (up to a dose of 420 mg) Medication taken until cGVHD progression, recurrence of an underlying malignancy, or unacceptable toxicity	Warnings/precautions Hemorrhage Infections Cardiac arrhythmias, cardiac failure, and sudden death Hypertension Cytopenias Second primary malignancies Hepatotoxicity Embryo-fetal toxicity Common AEs (=20%) Fatigue Anemia Bruising Diarrhea Thrombocytopenia Musculoskeletal pain Pyrexia Muscle spasms Stomatitis Hemorrhage Nausea Abdominal pain Pneumonia Headache
Ruxolitinib (Jakafi, Incyte)	Kinase inhibitor that targets JAK1 and JAK2, which regulate cytokine and growth factor signaling crucial for hematopoiesis and immune function. By blocking JAK/STAT signaling, it also modulates gene expression.	Intermediate- or high-risk myelofibrosis in adults Polycythemia vera in adults who have had an inadequate response to or are intolerant of hydroxyurea Steroid-refractory aGVHD in adult and pediatric patients =12 y cGVHD after failure of 1 or 2 lines of systemic therapy in adult and pediatric patients =12 y	Initial starting dose: 10 mg given orally twice daily For patients responding to treatment and who have stopped therapeutic corticosteroids, consider tapering ruxolitinib after 6 mo; reduce the dose gradually every 8 wk If GVHD symptoms reappear during or after tapering, consider restarting treatment	Warnings/precautions Thrombocytopenia, anemia, and neutropenia Infection Symptom exacerbation following interruption or discontinuation Non-melanoma skin cancer Lipid elevations MACE Thrombosis Secondary malignancies Common AEs Hematologic (=35%): anemia and thrombocytopenia Nonhematologic (=20%): infections and viral infections
AEs, adverse effects; aGVHD, acute graft-vs-host disease; BTK, Bruton’s tyrosine kinase; cGVHD, chronic GVHD; CLL, chronic lymphocytic leukemia; CSF-1R, colony-stimulating factor-1 receptors; JAK, Janus kinase; MACE, major adverse cardiovascular event; ROCK, rho-associated, coiled-coil containing protein kinase; SLL, small lymphocytic lymphoma; STAT, signal transducer and activator of transcription; WM, WaldenstrÖm’s macroglobulinemia. Based on references 16-19.

Ibrutinib

Ibrutinib, approved in 2017 for use in cGVHD after failure of 1 or more lines of systemic therapy, was evaluated in an open-label, phase 1b/2 trial in adult patients who failed to respond to first-line corticosteroids and required additional therapy.^16,20 The ORR for patients on ibrutinib was 67% (95% CI, 51%-80%), with sustained response for 20 or more weeks in 48% of patients and a median time to response of 12.3 weeks. In the open-label, phase 1/2 iMAGINE trial, the safety and efficacy of ibrutinib were evaluated in pediatric and young adult patients aged 1 year to less than 22 years.²¹ Fifty-nine patients (12 treatment-naive; 47 relapsed/refractory cGVHD) were enrolled. Safety outcomes aligned with ibrutinib’s known cGVHD profile. The overall ORR at 24 weeks was 64%, which included 83% in treatment-naive and 60% in relapsed/refractory patients. Among 46 responders, the 12-month duration of response was 60% (95% CI, 25%-83%) for treatment-naive and 58% (95% CI, 35%-75%) for relapsed/refractory patients.

Ruxolitinib

The FDA approved ruxolitinib in 2021 for patients with cGVHD after failure of 1 or 2 lines of systemic therapy.¹⁷ Its use was evaluated in the phase 3 randomized REACH-3 trial, which compared ruxolitinib with best available therapy in patients requiring additional treatment after corticosteroid failure.^17,22 Efficacy was based on the overall response rate (ORR) through cycle 7 day 1 of treatment (week 24). The overall difference in ORR between ruxolitinib and the best available arms (including ibrutinib, imatinib, infliximab, methotrexate, mTOR [mechanistic target of rapamycin] inhibitors, mycophenolate mofetil, pentostatin [Nipent, Hospira], or rituximab) was 13% (95% CI, 3%-23%); the median time to first response was 3 weeks with ruxolitinib.

Belumosudil

The 2021 approval of belumosudil was based on results from the open-label, phase 2 ROCKstar trial assessing the safety and efficacy of treatment in patients with cGVHD who had received 2 to 5 prior lines of systemic therapy.^18,23 The overall median follow-up duration was 14 months.²³ The best ORR for belumosudil at doses of 200 mg once daily and 200 mg twice daily were 74% (95% CI, 62%-84%) and 77% (95% CI, 65%-87%), respectively, with consistently strong responses seen across all subgroups. The median duration of response was 54 weeks, and 44% of participants continued treatment for at least 1 year.

Axatilimab-csfr

Axatilimab-csfr was approved in 2024 based on the results of the phase 2 AGAVE-201 trial.^19,24 The drug was evaluated at 3 different doses in 241 patients with recurrent/refractory cGVHD. An overall response occurred in 74% (95% CI, 63%-83%) of patients receiving the 0.3-mg dose, 67% (95% CI, 55%-77%) in the 1-mg group, and 50% (95% CI, 39%-61%) in the 3-mg group.²⁴ The median time to response across all dose groups was less than 8 weeks; among responders, an estimated 60% in both the 0.3- and 1-mg dose groups, and 53% in the 3-mg group, maintained a durable response at 12 months.

All 4 drugs received approval based on open-label, non-blinded trials, with only ruxolitinib being evaluated in a randomized study against best available therapy.⁵

Pharmacy Practice Considerations

Given the complexity of cGVHD, a multidisciplinary approach to patient care is critical. Pharmacists can play a key role in optimizing patient care through various interventions, including medication management, therapeutic drug monitoring (TDM), adverse effect monitoring, education, and counseling.²⁵

Medication expertise

When allogeneic HCT patients develop cGVHD, pharmacists can be vital in guiding therapeutic decisions alongside the care team for initial, and potential secondary and refractory, therapies.^2,26 As noted, there are many pharmacologic options for managing cGVHD.²⁶ Pharmacists are medication experts, and their education and training in pharmacology, drug safety, and formulation of pharmaceutical preparations can improve clinical outcomes by optimizing medication regimens.

Medication adherence

Patient medication burden can increase dramatically after allogeneic HCT and subsequent cGVHD.²⁵ Many of these medications may be dosed multiple times per day, which can result in a high pill burden and reduced medication adherence. For example, a recent systematic review (n=14 studies) on medication adherence among allogeneic HCT recipients found that the median medication adherence prevalence was 61.8% (61.5% for immunosuppressants [range, 31.3%-88.8%] and 65.2% for non-immunosuppressants [range, 48%-100%]).²⁷ Factors linked to nonadherence included younger age, higher psychosocial risk, distress, daily immunosuppressant use, and increased side effects. Four studies highlighted pharmacist-led interventions that improved medication adherence, while 2 studies linked medication nonadherence to prevalence of cGVHD. This highlights an opportunity for pharmacists in both the inpatient and outpatient settings to improve medication adherence in this patient population. More than 8,000 allogeneic HCTs are performed annually in the United States, and pharmacists need to be cognizant of targeted interventions to decrease nonadherence, such as patient education sessions, simplification of medication regimens, regular follow-up with healthcare providers, and technology-mediated adherence interventions.^25,28

Medication safety

Agents used in cGVHD also may require TDM, which presents an opportunity for pharmacists to assess and affect clinical outcomes of these medications.²⁵ Patients who have gone through allogeneic HCT may be on prophylactic antimicrobial (eg, aminoglycosides, vancomycin) and antifungal agents (eg, posaconazole, voriconazole), along with immunosuppressive therapies such as calcineurin inhibitors, methotrexate, and mycophenolate mofetil, which require serum level monitoring. These agents have a narrow therapeutic window, and targeted trough levels vary for calcineurin inhibitors such as cyclosporine (150-450 ng/mL), tacrolimus (5-20 ng/mL), and sirolimus (3-12 ng/mL).²⁹ Pharmacists can monitor and interpret pharmacokinetic parameters of these medications and dose-adjust as necessary to maintain adequate levels and reduce drug-related adverse reactions. Common drug-related adverse reactions for these agents include hepatotoxicity, neurotoxicity, and nephrotoxicity.

There also are available treatments to combat specific drug-induced adverse reactions. The mainstay of first-line treatment of cGVHD is steroids, and steroid use has been associated with short- and long-term adverse reactions including infection, hyperglycemia, bone loss, edema, and sleep/mood disturbances.⁷ Pharmacists can mitigate and minimize these side effects through recommendation of supportive care and symptom burden measures (eg, addition of anti-infectives, vaccination) or through the investigation of alternative therapies.²⁵

Other Considerations

Aside from clinical decision support and inpatient care interventions, pharmacists also play a significant role in ensuring safe transition of care for patients with cGVHD. This includes medication reconciliation at the time of inpatient admission and discharge and helping to facilitate access to cGVHD medications (eg, analysis of reimbursement issues, prior authorization assistance).²⁶ Medication reconciliation can help identify and evaluate appropriate indications, drug–drug interactions, and regimen effectiveness (eg, need for dose adjustments due to patient-specific factors, patient formulation preferences, and identification of adverse effects). Pharmacists can also play a crucial role in educating patients and other healthcare professionals on medication use during care transitions, ensuring proper administration, awareness of interactions, and potential side effects.²⁵ Pharmacists can collaborate with intensive care teams to align treatment goals, manage immunosuppressant levels, optimize antimicrobial dosing, and oversee lab monitoring, supporting informed decision-making. Pharmacists are also equipped to enhance patient comprehension of medication administration, missed doses, side effect management, and recognizing serious complications that require urgent care or follow-up.

Conclusion

Chronic GVHD is a complex and multifaceted disorder, which can have a significant impact on a patient’s quality of life. This condition presents many opportunities for pharmacists to ensure that patients with cGVHD receive optimal care in all phases of their care journey. Pharmacists can be an essential part of the multidisciplinary care team and help guide prevention and treatment strategies along with other interventions, such as drug monitoring, education, and counseling.

Dr. Munir reported no relevant financial disclosures.

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Optimizing Pharmacotherapy In Chronic GVHD: The Expanding Role of the Pharmacist

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