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Abaloparatide

✓ Approved; ATOM trial comparing with teriparatide
Abaloparatide (Tymlos; BA058)
Also known as: BA058, PTHrP(1-34) analog, Parathyroid hormone-related protein analog
Brand names: Tymlos
Page last reviewed

Quick Summary

Abaloparatide (Tymlos) is a synthetic 34-amino acid analogue of parathyroid hormone-related protein (PTHrP 1-34), FDA-approved in 2017 for postmenopausal osteoporosis at high fracture risk. Unlike teriparatide (which is PTH 1-34), abaloparatide is derived from PTHrP and incorporates 11 amino acid substitutions to optimize receptor selectivity.

Bone Anabolic Peptide FDA Approved
Abaloparatide (Tymlos) is a synthetic 34-amino acid analogue of parathyroid hormone-related protein (PTHrP 1-34), FDA-approved in 2017 for postmenopausal osteoporosis at high fracture risk. Unlike teriparatide (which is PTH 1-34), abaloparatide is derived from PTHrP and incorporates 11 amino acid substitutions to optimize receptor selectivity. Both PTH and PTHrP activate the PTH1R (type 1 PTH receptor), but abaloparatide exhibits preferential binding to the R0 conformation of PTH1R (a transient signaling state) versus the stable RG conformation favored by PTH/teriparatide. This receptor conformation selectivity is proposed to explain abaloparatide's more transient cAMP signaling, which may translate into relatively greater bone formation versus resorption stimulation compared to teriparatide, though clinical superiority over teriparatide has not been definitively established.
Storage Stability
Lyophilized
6–12 months (2–8°C)
Reconstituted
30 days (2–8°C)
Room temp
Stable (dry)

Mechanism of Action

PTH1R R0 Conformation Selectivity

Abaloparatide binds the PTH1R with a different receptor conformational selectivity than teriparatide. It preferentially stabilizes the R0 conformation (uncoupled from Gs protein), producing a more transient cAMP signal compared to teriparatide's prolonged cAMP via the RG conformation. This shorter cAMP pulse duration is hypothesized to favor osteoblast anabolic signaling (Wnt pathway, reduced osteoblast apoptosis) while minimizing prolonged RANKL-mediated osteoclast activation. Whether this translates to a clinically meaningful "anabolic window" advantage is debated.

Bone Formation and Remodeling

Like teriparatide, abaloparatide stimulates osteoblast differentiation, activity, and survival. Biochemical markers of bone formation (P1NP, osteocalcin) rise within 1-3 months. BMD increases are seen at spine (11% at 18 months in ACTIVE trial) and hip (4%). The ratio of bone formation to resorption markers at 3 months is more favorable for abaloparatide than teriparatide in head-to-head comparisons, potentially reflecting the proposed reduced resorptive drive.

Transient cAMP and Osteocyte Signaling

PTH1R on osteocytes regulates sclerostin production; receptor activation reduces sclerostin, lifting its inhibition of Wnt signaling and promoting bone formation throughout the skeleton. Abaloparatide's brief cAMP signal may reduce the rebound sclerostin increase that occurs between doses with teriparatide, potentially sustaining Wnt-driven bone formation more consistently across the 24-hour dosing interval.


Research Summary

ACTIVE Trial (Pivotal)

Standard of Care

The ACTIVE trial (n=2463, 18 months) showed abaloparatide 80 mcg/day reduced vertebral fractures by 86% and non-vertebral fractures by 43% versus placebo. Compared to the open-label teriparatide arm, abaloparatide showed numerically fewer non-vertebral fractures and similar vertebral fracture reduction. Spine BMD increased 11.2% vs 10.5% (teriparatide) and hip BMD increased 4.2% vs 3.2%, suggesting a modest hip BMD advantage.

ATOM Extension Trial

Clinical

The ATOM trial followed ACTIVE completers through 24 months of denosumab after abaloparatide or teriparatide. The abaloparatide-to-denosumab sequence produced greater total hip and femoral neck BMD gains than teriparatide-to-denosumab, suggesting abaloparatide may prime the skeleton for greater antiresorptive benefit when sequenced appropriately.

Hypercalcemia Comparison

Clinical

A notable finding was lower transient hypercalcemia with abaloparatide (3% grade 1) versus teriparatide (6% grade 1) in ACTIVE trial post-dose monitoring (1 hour after injection). This difference, attributed to reduced direct PTH1R-mediated calcium reabsorption in kidney (since abaloparatide binds R0 conformation with lower renal Ca reabsorption), is a potential tolerability advantage in patients with calcium metabolism concerns.


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Research Protocols

GoalDoseFrequencyRoute
Osteoporosis treatment80 mcg SC once dailyOnce daily; maximum 2 years cumulativeSC (periumbilical abdomen)
Head-to-head vs teriparatide (ATOM)80 mcg SC abaloparatide vs 20 mcg SC teriparatideOnce daily x 18 months then denosumabSC injection
PTH1R conformation study1-1000 nM in receptor binding assaySingle concentration-responseIn vitro receptor preparation

Rotate injection sites. Sit or lie down for 30 minutes after injection (hypotension risk). Monitor calcium at 1 and 3 months. Follow with antiresorptive (bisphosphonate or denosumab) to preserve gains.


Interactions

Do not combine
Teriparatide
Both activate PTH1R; combining provides no additional benefit and increases adverse effect risk
Sequential
Denosumab
Abaloparatide then denosumab (ATOM protocol) provides greater total BMD gains than either alone
Sequential
Bisphosphonates
Concurrent bisphosphonates blunt abaloparatide anabolic response; use sequentially (abaloparatide first)
Required
Calcium / Vitamin D
Adequate calcium and vitamin D intake essential for anabolic response; supplement if dietary intake inadequate

Safety Profile

Abaloparatide's adverse effect profile is similar to teriparatide with some differences. Hypercalcemia is less frequent (3% vs 6% for teriparatide at 1 hour post-dose). Orthostatic hypotension and dizziness occur in the hour post-injection, patients should sit or lie down for 30 minutes. Nausea, fatigue, and injection site reactions (pain, erythema) are common. Osteosarcoma risk carries the same black box warning as teriparatide (based on rat studies at supraphysiological doses; not observed in humans). Contraindicated in hypercalcemia, Paget disease, open epiphyses, and prior skeleton irradiation.


References

  • [1]Miller PD, et al. Effect of abaloparatide vs placebo on new vertebral fractures in postmenopausal women with osteoporosis: a randomized clinical trial (ACTIVE). JAMA. 2016;316:722-733.
  • [2]Leder BZ, et al. Denosumab and teriparatide transitions in postmenopausal osteoporosis (the DATA-Switch study). Lancet. 2015.
  • [3]Hattersley G, et al. Differentiating abaloparatide and teriparatide by their actions on the PTH1R receptor. J Bone Miner Res. 2016.
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Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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