The Pharmaceutical Benefits Scheme (PBS) listing for triptorelin 3.75 mg has expanded with the addition of an unrestricted benefit. This allows subsidised access in a number of women’s health conditions, which may provide reassurance to patients affected by the planned delisting of Zoladex® (goserelin) 3.6 mg.
Triptorelin is a gonadotrophin releasing hormone (GnRH) agonist. The 3.75 mg presentation is administered once a month as a single intramuscular injection. Initial administration results in a transient increase in luteinising hormone (LH), follicle stimulating hormone (FSH), and sex hormone production. Continued administration leads to suppression of LH and FSH secretion, resulting in reduced production of sex hormones. Common adverse effects include hot flushes, headache, and mood changes.
The expanded PBS listing for triptorelin 3.75 mg improves subsidised access for women requiring treatment with a GnRH agonist. With the delisting of Zoladex® (goserelin) 3.6 mg currently scheduled for May 2027, triptorelin is an alternative monthly GnRH agonist that may be considered. Although both medicines have a similar mechanism of action, healthcare professionals should be aware of differences in formulation and administration, as shown in Table 1.
| Feature |
Triptorelin 3.75 mg |
Goserelin 3.6 mg |
| Presentation |
Vial (powder for suspension) |
Pre-filled syringe |
| Route |
Intramuscular |
Subcutaneous implant |
| PBS criteria |
Unrestricted benefit |
Prostate cancer, breast cancer, endometriosis, anticipated premature ovarian failure (chemotherapy induced).
* Scheduled for delisting in May 2027. |
From October 1 2026, tacrolimus 0.1% ointment will be available on the Pharmaceutical Benefits Scheme (PBS) for the treatment of atopic dermatitis. Eligible patients must be at least 16 years of age and have moderate to severe disease.
Tacrolimus is a calcineurin inhibitor that suppresses T-cell activation and cytokine production. It also inhibits the release of inflammatory mediators from skin mast cells and basophils. Although topical corticosteroids remain the cornerstone of drug treatment for atopic dermatitis, non-steroid options may be appropriate for some patients.
A large meta-analysis comparing topical treatments for atopic dermatitis found tacrolimus 0.1% ointment to be among the most effective of the therapies evaluated for reducing itch severity and preventing flare-ups. Comparative studies have also shown tacrolimus to be more effective than pimecrolimus cream, with a faster onset of action. However, pimecrolimus remains an effective alternative, and some patients may prefer its cream formulation.
Tacrolimus may be used for the short-term treatment of acute flares. Intermittent long-term use may be considered in select patients to reduce recurrence and prolong flare-free periods. The most common adverse effects are application-site reactions such as burning, stinging, itching, and warmth. These effects are usually mild to moderate and tend to lessen as skin inflammation improves. Alcohol intolerance, which may present as facial flushing or skin irritation after alcohol consumption, has also been reported. Unlike topical corticosteroids, tacrolimus does not cause skin atrophy, striae, or telangiectasia, making it particularly useful for delicate skin areas and for patients requiring repeated courses of treatment.
From 1 September 2026, the Pharmaceutical Benefits Scheme (PBS) listing for pembrolizumab was significantly expanded with the addition of a multi-cancer listing. The new listing provides subsidised access for patients with immunotherapy sensitive advanced or metastatic cancer.
Pembrolizumab is an immunotherapy that acts as an inhibitor of programmed cell death protein-1 (PD-1). Tumour cells can exploit the PD-1 pathway to evade immune detection. By blocking this pathway, pembrolizumab can enhance anti-tumour immune responses.
Pembrolizumab is administered as an intravenous infusion over 30 minutes. Dosing varies according to indication, with treatment typically given every three or six weeks. Immune-mediated adverse reactions are common and can affect almost any organ system. Potential immune-mediated reactions include pneumonitis, colitis, nephritis, hepatitis, and various endocrinopathies. Infusion-related reactions may also occur and can include rigors, chills, wheezing, pruritus, flushing, rash, hypotension, and fever. These reactions are typically mild to moderate and premedication may be considered in selected patients. Severe or life-threatening infusion-related reactions are rare but require permanent discontinuation.
This recent PBS update allows pembrolizumab to be subsidised based on tumour characteristics rather than the cancer’s tissue of origin, potentially improving access for patients with a broader range of advanced cancers.
Abaloparatide is now listed on the Pharmaceutical Benefits Scheme (PBS) for severe osteoporosis in both first-line and second-line settings.
Abaloparatide acts as an agonist at the parathyroid hormone receptor 1 (PTHR1) to stimulate osteoblast activity. As it promotes new bone formation, abaloparatide is classified as an anabolic osteoporosis therapy. In comparison, antiresorptive medications (such as bisphosphonates) primarily slow bone resorption. For patients at very high fracture risk, the early use of anabolic therapy is increasingly recognised as an effective strategy to rapidly improve bone strength and reduce fracture risk.
The phase 3 ACTIVE trial randomised 2,463 postmenopausal women with osteoporosis to receive daily subcutaneous abaloparatide, teriparatide, or placebo for 18 months. Abaloparatide significantly reduced the incidence of new vertebral fractures compared with placebo (0.6% vs 4.2%), as well as nonvertebral fractures (2.7% vs 4.7%). In addition, abaloparatide was associated with increases in bone mineral density (BMD) at the lumbar spine, total hip, and femoral neck. Gains in BMD were significantly greater than those seen with teriparatide at the total hip and femoral neck at all time points studied. Abaloparatide was generally well tolerated, with rates of serious adverse events similar to placebo and teriparatide. The incidence of hypercalcaemia was significantly lower with abaloparatide than with teriparatide (3.4% vs 6.4%).
Abaloparatide is administered as a once-daily subcutaneous injection. Treatment is limited to a maximum duration of 18 months as animal studies indicate an increased risk of osteosarcoma with prolonged exposure. While the relevance of these findings to humans is uncertain, abaloparatide is contraindicated in patients with a known risk of osteosarcoma. As with other anabolic osteoporosis therapies, treatment may be followed by an antiresorptive agent to maintain BMD gains and sustain fracture risk reduction.
From 1 August 2026, vorasidenib is available on the Pharmaceutical Benefits Scheme (PBS) for eligible patients with grade 2 IDH-mutant astrocytoma or oligodendroglioma. It is the first new treatment in more than 20 years for these rare brain tumours and the first targeted therapy approved in Australia for this patient population.
Vorasidenib is an oral therapy that inhibits mutant isocitrate dehydrogenase (IDH) 1 and IDH2 enzymes. Mutations in these enzymes can promote tumour growth through the production of the oncometabolite 2-hydroxyglutarate (2-HG).
Grade 2 IDH-mutant gliomas are rare, slow-growing brain tumours that typically affect younger adults. Management typically involves surgical resection. This may be followed by radiotherapy and chemotherapy, although active surveillance may be appropriate for low-risk patients.
The double-blind phase III INDIGO trial enrolled patients with residual or recurrent grade 2 IDH-mutant astrocytoma or oligodendroglioma who had undergone surgery as their only previous treatment. Compared with placebo, patients in the vorasidenib group demonstrated significantly prolonged progression-free survival (median 27.7 months vs. 11.1 months) and delayed need for subsequent interventions.
Common adverse effects reported with vorasidenib include fatigue, headache, diarrhoea, nausea, and elevated liver enzymes. Liver function should be monitored regularly during treatment, particularly during the first year of therapy, due to the risk of hepatotoxicity.
The Therapeutic Goods Administration (TGA) has released a safety alert regarding the risk of eye disorders with glucagon-like peptide-1 (GLP-1) analogues. These medicines are used in the management of type 2 diabetes mellitus and obesity, and include:
- Dulaglutide (Trulicity®)
- Semaglutide (Ozempic®, Wegovy®)
- Liraglutide
- Tirzepatide (Mounjaro®)*
*Note: Tirzepatide is a dual glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 analogue.
Product Information (PI) documents for these medicines have been updated to include a warning regarding the risk of non-arteritic anterior ischaemic optic neuropathy (NAION). This is a rare but serious eye disorder caused by reduced blood flow to the optic nerve. It typically presents with sudden and painless loss of vision in one eye and can result in permanent visual impairment or blindness. Current evidence more strongly supports an association with semaglutide; however, warnings have been added for all agents in the class.
Although the risk of NAION appears to be very low, healthcare professionals should be aware of this emerging safety signal given the increasing use of GLP-1 analogues and the potential severity of the outcome. Patients should be advised to seek urgent medical assessment if they experience any unexplained changes in vision. Suspected cases of NAION should be reported to the TGA to support ongoing safety monitoring.
Rozanolixizumab is now available on the Pharmaceutical Benefits Scheme (PBS) for the treatment of generalised myasthenia gravis. Myasthenia gravis is an autoimmune disorder characterised by fluctuating muscle weakness and fatigability.
Rozanolixizumab is a monoclonal antibody that blocks the neonatal Fc receptor (FcRn). FcRn normally protects immunoglobulin G (IgG) antibodies and albumin from intracellular degradation, thereby extending their circulating half-life. By preventing FcRn from salvaging and recycling IgG antibodies, rozanolixizumab promotes their lysosomal degradation. This rapidly reduces the levels of circulating IgG, including pathogenic autoantibodies.
Rozanolixizumab is administered as a subcutaneous infusion. In the Phase 3 MycarinG trial, patients were randomly assigned to receive weekly infusions of rozanolixizumab 7 mg/kg, rozanolixizumab 10 mg/kg, or placebo for six weeks. The primary efficacy endpoint was change from baseline in the Myasthenia Gravis Activities of Daily Living (MG-ADL) score. Higher scores indicate greater disability and a reduction of at least 2 points is generally considered clinically meaningful. Mean reductions in MG-ADL score were greater with rozanolixizumab 7 mg/kg (-3.37) and 10 mg/kg (-3.40) than with placebo (-0.78).
The most commonly reported adverse effects were headache, diarrhoea, and pyrexia. While formal drug interaction studies have not been conducted, rozanolixizumab is expected to affect IgG-based therapies. If intravenous immunoglobulin (IVIg) or monoclonal antibody therapies are required, it is recommended that they be initiated at least two weeks after a rozanolixizumab infusion and that patients be monitored for reduced therapeutic efficacy.
Insulin degludec (Tresiba®) is now available on the Pharmaceutical Benefits Scheme (PBS) for the treatment of type 1 diabetes mellitus.
Tresiba® is an ultra-long-acting basal insulin analogue with a duration of action of at least 42 hours. It is intended for once daily administration and may be given at any time of the day. While patients should be encouraged to administer doses at around the same time each day, the slow and consistent rate of absorption allows some dosing flexibility.
The SWITCH 1 and SWITCH 2 trials compared insulin degludec with insulin glargine (U100) in patients with type 1 and type 2 diabetes, respectively. Post hoc analysis of these trials found that improved glycaemic control increased hypoglycaemia risk regardless of the basal insulin used. However, for equivalent HbA1c reductions, degludec was associated with smaller increases in hypoglycaemia than glargine in both populations. These findings suggest that degludec may help patients achieve lower HbA1c targets with a lower risk of hypoglycaemia.
The PBS listing of degludec provides an additional basal insulin option for patients affected by the planned discontinuation of insulin detemir (Levemir®) from the Australian market later this year.
The Pharmaceutical Benefits Scheme (PBS) listing for acalabrutinib has been expanded to include the first-line treatment of chronic lymphocytic leukaemia (CLL) or small lymphocytic lymphoma (SLL) in combination with venetoclax. Patients receive acalabrutinib monotherapy for the first two cycles, followed by combination therapy with venetoclax from cycle three.
Acalabrutinib is a second-generation Bruton’s tyrosine kinase (BTK) inhibitor. In B-cells, BTK signalling drives B-cell proliferation, trafficking, chemotaxis, and adhesion. Venetoclax is a selective inhibitor of B-cell lymphoma-2 (BCL-2), a protein that regulates apoptosis and is often overexpressed in CLL and SLL.
Both acalabrutinib and venetoclax are administered orally with a fixed dosing period of 14 cycles for this indication (where each cycle is 28 days). Acalabrutinib is taken twice daily, while venetoclax is taken daily from cycle three. A five-week ramp-up schedule is employed for venetoclax to gradually reduce tumour burden and lower the risk of tumour lysis syndrome.
The AMPLIFY trial was conducted in patients with untreated CLL. Combination therapy with acalabrutinib and venetoclax was associated with significantly prolonged progression-free survival compared with chemoimmunotherapy. Common adverse events included infection, neutropenia, and haemorrhage. Acalabrutinib has a more favourable cardiovascular safety profile than first-generation BTK inhibitors such as ibrutinib; however, hypertension and atrial fibrillation can still occur.
The Paxlovid® product information has recently been updated; it is no longer contraindicated in severe renal impairment.
Paxlovid® is an oral antiviral therapy for COVID-19 that contains nirmatrelvir co-packaged with ritonavir. Nirmatrelvir is a SARS-CoV-2 protease inhibitor that prevents viral replication, while ritonavir inhibits its hepatic metabolism. Co-administration is required to ensure plasma levels of nirmatrelvir reach the target therapeutic range.
When administered with ritonavir, renal excretion becomes the primary route of elimination for nirmatrelvir. Systemic exposure increases as renal function declines. A small open label study evaluated the safety of nirmatrelvir and ritonavir in patients with severe renal impairment. Findings suggest similar safety and efficacy to that observed in placebo-controlled trials that excluded patients with moderate to severe renal impairment.
No dose adjustment is required in mild renal impairment. However, dose reduction is recommended for patients with moderate and severe renal impairment, as outlined in Table 1.
Table 1. Recommended dose adjustments in renal impairment
| eGFR (mL/min/1.73m2) |
Nirmatrelvir |
Ritonavir |
Frequency |
| ≥60 |
300mg |
100mg |
12-hourly |
| ≥30 to <60 |
150mg |
100mg |
12-hourly |
| <30 |
300mg |
100mg |
Once on Day 1 |
| 150mg |
100mg |
Daily from Day 2 |
Abbrev: eGFR, estimated glomerular filtration ratePatients with severe renal impairment are at increased risk of severe COVID-19 outcomes, including hospitalisation and death. Therefore, access to appropriately dose-adjusted antiviral therapy is important. Patients receiving dose-adjusted Paxlovid® should be provided with clear dosing instructions and advised that the pack provided may contain more tablets than required for their course.
