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  1. pharmadog
  2. ›drugs
  3. ›Alyftrek
drug
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(deutivacaftor + tezacaftor + vanzacaftor calcium)

Marketedupdated 5mo ago
by $VERX Vertex, Inc.
Approved
community read0 votes

🐶 often sniffed alongside

top 3
  • drugALYFTREK8 co-mentions · 4 sources
  • tagApproval8 co-mentions · 4 sources
  • tagSmall Molecule4 co-mentions · 4 sources

Small molecule drug with a maximum clinical stage of Approval, with an approval for cystic fibrosis.

indications

investigational
Cystic Fibrosis

all catalysts(4)

approval · 4
Dec 20, 2024
approval
$VERX12.22+3.78%
2y ago
ALYFTREK (DEUTIVACAFTOR) — FDA approval
(deutivacaftor + tezacaftor + vanzacaftor calcium)
→
Sep 25, 2025
approval
$VERX12.22+3.78%
1y ago
ALYFTREK (DEUTIVACAFTOR) — FDA approval
(deutivacaftor + tezacaftor + vanzacaftor calcium)
→
Mar 17, 2026
approval
$VERX12.22+3.78%
7mo ago
ALYFTREK (DEUTIVACAFTOR) — FDA approval
(deutivacaftor + tezacaftor + vanzacaftor calcium)
→
Mar 27, 2026
approval
$VERX12.22+3.78%
6mo ago
ALYFTREK (DEUTIVACAFTOR) — FDA approval
(deutivacaftor + tezacaftor + vanzacaftor calcium)
→

Patent cliff

source: FDA Orange Book
first barrier falls
Dec 28, 2026
86 days

Earliest of all listed patents + FDA exclusivities. Generic / biosimilar entry typically only becomes possible AFTER both patent and exclusivity barriers expire.

patents (61)

  • Jan 10, 2043method-of-use (U-4088)US 12186306
  • Aug 13, 2040compositionUS 11873300
  • Aug 13, 2040compositionUS 11873300
  • Feb 14, 2039compositionUS 11066417
  • Feb 14, 2039compositionUS 11066417
  • Feb 14, 2039method-of-use (U-4082)US 11866450
  • Feb 14, 2039method-of-use (U-4082)US 11866450
  • Apr 14, 2035formulationUS 10206877
  • Apr 14, 2035formulationUS 11951212
  • Jul 15, 2033method-of-use (U-4218)US 10058546
  • Jul 15, 2033method-of-use (U-4097)US 9012496
  • May 17, 2032compositionUS 10047053
  • May 17, 2032compositionUS 10047053
  • May 17, 2032compositionUS 8865902
  • May 17, 2032compositionUS 8865902
  • May 17, 2032compositionUS 9181192
  • May 17, 2032compositionUS 9181192
  • May 17, 2032compositionUS 9512079
  • May 17, 2032compositionUS 9512079
  • Jul 10, 2031compositionUS RE504534.8y
  • Jul 10, 2031compositionUS RE504534.8y
  • Mar 25, 2031formulationUS 100816214.5y
  • Mar 25, 2031formulationUS 100816214.5y
  • Mar 25, 2031formulationUS 115780624.5y
  • Mar 25, 2031formulationUS 115780624.5y
  • Aug 13, 2029formulationUS 106464812.9y
  • Aug 13, 2029formulationUS 106464812.9y
  • Aug 13, 2029method-of-use (U-4095)US 115649162.9y
  • Aug 13, 2029method-of-use (U-4095)US 115649162.9y
  • Nov 12, 2027method-of-use (U-4082)US 84153871.1y
  • Nov 12, 2027method-of-use (U-4082)US 84153871.1y
  • Aug 5, 2027method-of-use (U-4090)US 8324242306d
  • Aug 5, 2027method-of-use (U-4090)US 8324242306d
  • Jun 3, 2027compositionUS 7776905243d
  • Jun 3, 2027compositionUS 7776905243d
  • May 20, 2027compositionUS 7495103229d
  • May 20, 2027compositionUS 7495103229d
  • May 1, 2027compositionUS 7645789210d
  • May 1, 2027compositionUS 7645789210d
  • May 1, 2027method-of-use (U-4090)US 8598181210d
  • May 1, 2027method-of-use (U-4090)US 8598181210d
  • May 1, 2027compositionUS 8623905210d
  • May 1, 2027compositionUS 8623905210d
  • Apr 9, 2027formulationUS 10022352188d
  • Apr 9, 2027formulationUS 10022352188d
  • Apr 9, 2027compositionUS 10239867188d
  • Apr 9, 2027compositionUS 10239867188d
  • Apr 9, 2027compositionUS 11639347188d
  • Apr 9, 2027compositionUS 11639347188d
  • Apr 9, 2027formulationUS 9974781188d
  • Apr 9, 2027formulationUS 9974781188d
  • Dec 28, 2026formulationUS 841027486d
  • Dec 28, 2026formulationUS 841027486d
  • Dec 28, 2026compositionUS 875422486d
  • Dec 28, 2026compositionUS 875422486d
  • Dec 28, 2026formulationUS 967016386d
  • Dec 28, 2026formulationUS 967016386d
  • Dec 28, 2026formulationUS 993133486d
  • Dec 28, 2026formulationUS 993133486d
  • Jul 6, 2026method-of-use (U-4091)US 8354427
  • Jul 6, 2026method-of-use (U-4091)US 8354427

FDA exclusivities (2)

  • Dec 20, 2029NCENew Chemical Entity (5y)3.2y
  • Dec 20, 2029NCENew Chemical Entity (5y)3.2y

News(5)

  • ReCode CEO Suliman leaves cystic fibrosis mission in mentee’s hands
    After achieving clinical validation earlier this year, ReCode Therapeutics has called up a new CEO to take on the mission of advancing programs for cystic fibrosis and primary ciliary dyskinesia th…
    biospace · 9d ago
  • Lilly pens $370M deal with OmniAb for ion channel collab, but details remain vague
    Antibody platform business OmniAb continues to rack up Big Pharma partnerships, with Eli Lilly signing off on up to $370 million biobucks tied to an ion channel program.
    fiercebiotech · 1mo ago
  • Sionna’s cystic fibrosis failure is a windfall for Vertex’s blockbuster franchise
    A surprise flop in Phase 2a cystic fibrosis trial sent Sionna’s shares plummeting, but for Vertex, the news reinforced its standard-of-care standing with highly successful drugs like Trikafta.
    biospace · 1mo ago
  • Vertex’s biggest overhang: a rival 50 times smaller
    Despite another strong earnings report, analysts warned that upcoming cystic fibrosis data from Sionna Therapeutics "looms large" over Vertex.
    biopharma_dive · 1mo ago
  • Vertex earnings get muted investor response
    While overall revenue fell just shy of Wall Street forecasts, sales of the gene editing medicine Casgevy and pain drug Journavx missed analyst estimates by double-digit percentages.
    biopharma_dive · 5mo ago
brand
Alyftrek
generic
(deutivacaftor + tezacaftor + vanzacaftor calcium)
MOA
12.1 Mechanism of Action Vanzacaftor and tezacaftor bind to different sites on the CFTR protein and have an additive effect in facilitating the cellular processing and trafficking of select mutant forms of CFTR (including F508del- CFTR) to increase the amount of CFTR protein delivered to the cell surface compared to either molecule alone. Deutivacaftor potentiates the channel open probability (or gating) of the CFTR protein at the cell surface. The combined effect of vanzacaftor, tezacaftor and deutivacaftor is increased quantity and function of CFTR at the cell surface, resulting in increased CFTR activity as measured both by CFTR-mediated chloride transport in vitro and by sweat chloride in patients with CF. CFTR Chloride Transport Assay in Fischer Rat Thyroid Cells Expressing Mutant CFTR Protein Effects of vanzacaftor/tezacaftor/deutivacaftor on chloride transport for mutant CFTR protein was determined in Ussing chamber electrophysiology studies using a panel of Fischer Rat Thyroid (FRT) cell lines stably expressing CFTR protein from individual variants. Vanzacaftor/tezacaftor/deutivacaftor increased chloride transport in FRT cells expressing select CFTR variants, as identified in Table 5. The threshold that the treatment-induced increase in chloride transport must exceed for the mutant CFTR protein to be considered responsive is ≥10% of normal over baseline. This threshold was used because it is expected to predict clinical benefit. For individual variants, the magnitude of the net change over baseline in CFTR-mediated chloride transport in vitro is not correlated with the magnitude of clinical response. CFTR Chloride Transport Assay in Human Bronchial Epithelial Cells Expressing Mutant CFTR Protein Homozygous and heterozygous N1303K- Human Bronchial Epithelial (HBE) cells showed greater chloride transport in the presence of vanzacaftor/tezacaftor/deutivacaftor than F508del/F508del- HBE cells treated with tezacaftor/ivacaftor which has shown clinical benefit in
indication
Cystic Fibrosis
phase
marketed
Data sources
openFDA · ClinicalTrials.gov
last refreshed 4h ago
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