Systemic
DeLLphi-304 (tarlatamab CNS outcomes)
For2L ES-SCLC; brain mets subgroup β₯1 BM at baseline, >70% prior CNS treatment
TL;DRCNS PFS HR 0.54 (ITT), HR 0.40 in brain mets; CNS CR 14.9% vs 5.4% with tarlatamab vs chemo 2L SCLC.
- DeLLphi-304 primary results: tarlatamab OS + PFS benefit in 2L SCLC; CNS data extends intracranial signal
| Arm | n | Median CNS PFS (mo) | HR (95% CI) |
|---|---|---|---|
| Tarlatamab | 67 | 6.5 (4.3-13.7) | 0.40 (0.24-0.66) |
| Chemotherapy | 56 | 4.2 (2.9-5.5) | ref |
+2 more figures
| Arm | n | Median CNS PFS (mo) | HR (95% CI) |
|---|---|---|---|
| Tarlatamab | 254 | NE (13.7, NE) | 0.54 (0.39-0.75) |
| Chemotherapy | 255 | 7.2 (5.6, NE) | ref |
| Endpoint | Tarlatamab (n=67) | Chemo (n=56) |
|---|---|---|
| CNS CR | 10 (14.9%) | 3 (5.4%) |
| Non-CR/Non-PD | 42 (62.7%) | 37 (66.1%) |
| CNS DCR | 52 (77.6%) | 40 (71.4%) |
| Median duration CNS CR (mo) | NE | 3.6 |
| Median duration CNS DC (mo) | 8.2 | 5.2 |
5 details
- π Post-hoc subgroup analysis of DeLLphi-304 phase 3 RCT; ITT n=509 (254 tarlatamab / 255 chemo)
- π Brain mets subgroup: n=67 (tarlatamab) vs n=56 (chemo); >70% had prior CNS treatment
- π Data cutoff Jan 29 2025; median f/u 11.4 mo (tarlatamab), 11.5 mo (chemo)
- π Ongoing CNS complete response at cutoff: 5 (50%) tarlatamab vs 0 chemo
- β οΈ CNS outcomes not prespecified; interpretability limited without a confirmatory prospective CNS endpoint
- Does tarlatamab CNS activity change the role of PCI in ES-SCLC?
- Confirmatory prospective CNS endpoint needed from DeLLphi-304 or successor trial
- Durability of CNS CR beyond 11mo median f/u
π Sources Β· π¦ 1 tweet
Dr. @g_mountzios #ASCO26 presents CNS outcomes with 2L tarlatamab in DeLLphi-304. Improved time to CNS progression overall (HR 0.54). In pts with brain nets, tarlatamab vs chemo CNS CR rate 15% vs 5% with DCR 78% vs 71% and time to CBS progression 6.5m vs 4.2m, HR 0.40 pic.twitter.com/5i8jL1zlKW
— Stephen V Liu, MD (@StephenVLiu) June 1, 2026
PROTEUS
ForBiochemically recurrent prostate cancer, post-radical prostatectomy
TL;DR53.0% (APA) and 60.7% (ADT) of MFS events PSMA PET-detected; APA+ADT vs ADT benefit in BCR prostate hotly contested.
6 details
- π Phase 3 RCT, APA + ADT vs ADT alone in BCR prostate cancer, post-RP setting
- π Full primary endpoint data pending ASCO26 presentation; no effect size reported in source tweets
- π NEJM paper: 53.0% (APA arm) and 60.7% (ADT arm) of distant mets identified by PSMA PET, not conventional imaging
- β οΈ Majority of MFS events PSMA PET-only: magnitude of conventional-imaging MFS benefit unclear
- β οΈ ASCO26 preview framing: 'some may call this a homerun, others may call this the largest negative'
- β PSMA PET-detected MFS not an established OS surrogate; does EFS benefit translate to survival?
- Does PSMA PET-detected EFS/MFS benefit translate to OS?
- Magnitude of benefit by conventional imaging alone
π Sources Β· π¦ 3 tweets
#ASCO26
— Daniel E Spratt (@DrSpratticus) May 31, 2026
The PROTEUS trial results are now online...buckle up as we wait to see the full presentation. This is going to be a trial that is likely highly controversial until the full results are published.
Some may call this a homerun, others may call this the largest negativeβ¦
Thought experiment:
— Sean McBride (@seanmmcbride) May 31, 2026
Let's take a very simple hypothetical trial involving 100 patients in the APA arm and 100 patients in the ADT alone arm. Pulling from PROTEUS EFS data, assume that, by 5 years, 60 patients in the ADT arm have had a BCR compared to 50 in the ADT+APA arm.β¦ pic.twitter.com/WJaiDlJnQs
#ASCO26
— Daniel E Spratt (@DrSpratticus) May 31, 2026
Talk about real-time updates. NEJM paper now online and my predictions and inferences appear true.
Majority of MFS events were by PET not conventional imaging. "Most distant metastases were identified by PSMA PET (53.0% of those in the apalutamide group and 60.7% in the⦠https://t.co/Yz4myY0flq
ENZARAD
ForHigh-risk localized PCa (Gleason 8-10, T3-4, or N1, or PSA β₯20 ng/mL), suitable
TL;DRMFS HR 0.88 (p=0.34), OS HR 0.87 (p=0.40); enzalutamide added to RT+2y ADT did not improve outcomes in high-risk localized PCa.
| Arm | Events/N | MFS 8y | HR (95% CI) | 2p |
|---|---|---|---|---|
| Enzalutamide | 98/401 | 74% | 0.88 (0.67-1.15) | 0.34 |
| Control (NSAA) | 109/401 | 72% | ref | ref |
+2 more figures
| Arm | Events/N | OS 8y | HR (95% CI) | 2p |
|---|---|---|---|---|
| Enzalutamide | 69/401 | 83% | 0.87 (0.63-1.20) | 0.40 |
| Control (NSAA) | 77/401 | 80% | ref | ref |
5 details
- π Phase 3 RCT (ANZUP), N=802, 1:1; high-risk localized PCa (Gleason 8-10, T3-4, N1, or PSA β₯20 ng/mL); median FU 8y
- π Enzalutamide 160mg/d x24mo + LHRH agonist x24mo vs NSAA x6mo + LHRH agonist x24mo; both arms: RT Β± brachytherapy boost Β± pelvic nodal RT
CONSORT flow
- π Both 1Β° (MFS) and 2Β° (OS) endpoints not met; overall trial negative
- β οΈ Pelvic RT and cN1 subgroup interactions are exploratory in a negative trial; hypothesis-generating, not sufficient for practice change
- β οΈ ICECAP surrogacy framework cited validating MFS as OS surrogate; both concordantly null, no hidden OS benefit suggested
- Whether pelvic RT selection prospectively enriches for ARSI benefit in high-risk localized PCa
- Optimal ADT intensification strategy for cN1 high-risk prostate cancer
π Sources Β· π¦ 1 tweet
π¨ENZARAD at #ESMO25 presented by @DrPaulNguyen
— Pierre Blanchard, MD (@PBlanchardMD) October 19, 2025
No improvement in MFS or OS with the addition of enzalutamide to high dose radiotherapy + 2y ADT in high risk #prostatecancer
Possible benefit in cN1 pts or pts treated with pelvic RT. pic.twitter.com/vXLRKuIPeg
RASolute 302
ForPrev-treated metastatic PDAC, RAS G12 mutation, β₯1 prior systemic line
TL;DRDaraxonrasib vs IC chemo in 2L RAS G12 mPDAC: mOS 13.2 vs 6.6 mo, HR 0.40 (0.30-0.54), p<0.001.
- 2L PDAC historical: IC chemo (FOLFOX, nalirinotecan-based regimens) mOS ~5-7 mo; daraxonrasib more than doubles median in RAS G12-selected pts
| Daraxonrasib | Chemotherapy | |
|---|---|---|
| RAS G12: N | 228 | 231 |
| RAS G12: mOS (95% CI) | 13.2 mo (10.0-NR) | 6.6 mo (5.4-8.2) |
| RAS G12: HR (95% CI), p | 0.40 (0.30-0.54), p<0.001 | ref |
| RAS G12: 12-mo OS | 53.3% | 8.7% |
| Overall: N | 248 | 252 |
| Overall: mOS (95% CI) | 13.2 mo (10.0-NR) | 6.7 mo (5.8-8.0) |
| Overall: HR (95% CI), p | 0.40 (0.30-0.53), p<0.001 | ref |
| Overall: 12-mo OS | 53.2% | 17.3% |
6 details
- π Phase 3 RCT; RAS G12 primary analysis N=459 (228 vs 231); overall N=500 (248 vs 252); control: investigator's choice chemotherapy
CONSORT flow
- π 1Β° EP (RAS G12 population): mOS 13.2 mo (95% CI 10.0-NR) vs 6.6 mo (5.4-8.2); HR 0.40 (0.30-0.54), p<0.001
- π 12-mo OS (RAS G12): 53.3% daraxonrasib vs 8.7% chemo
- π Consistent in overall population (all RAS mutations + no-mutation pts, N=500): HR 0.40 (0.30-0.53), p<0.001; mOS 13.2 vs 6.7 mo
- β οΈ Event maturity asymmetric at datacut: 32% events in daraxonrasib arm vs 55% chemo; upper OS CI not reached (NR); follow-up ongoing
- β οΈ G12 variant breakdown (G12D vs G12V vs G12R) not reported in source
- Activity by specific G12 variant (G12D vs G12V vs G12R)
- Durability beyond current f/u; upper OS CI not yet reached
- Optimal sequencing and potential 1L investigation
π Sources Β· π¦ 1 tweet
#ASCO26
— Nicholas Hornstein (@GIMedOnc) May 31, 2026
This one is special.
This is the hottest paper of 2026 and potentially in the history of pancreatic cancer.
Letβs dive in.
RASolute 302: Daraxonrasib vs investigatorβs choice chemotherapy in previously treated metastatic pancreatic cancer
Abstract LBA5 (soon!)β¦ pic.twitter.com/Lq7PEjOWAo
A-DREAM (ALLIANCE mAPMS)
FormHSPC achieving PSA<0.2 after β₯18-24mo ADT+ARPI, low-volume predominant
TL;DRADT+ARPI interruption in mHSPC: 41% treatment-free with eugonadal T at 18mo (1Β° EP); 38.5% still off-tx at 26.9mo FU.
- Intermittent ADT established in earlier hormone-sensitive trials; A-DREAM is first prospective signal for ADT+ARPI interruption in mHSPC
+2 more figures
9 details
- π Single-arm phase II, N=78 enrolled 07/2022-03/2024; PSA<0.2 after β₯18-24mo ADT + β₯12mo ARPI
- π Re-initiation triggers: PSA β₯5 ng/mL, radiographic change (PCWG3), or PrCa-related sx
- π Primary EP: 80% CI 33.1-48.9%, one-sided p=0.0249; pre-specified 80% CI threshold (not 95%)
- π Median time to eugonadal T recovery: 9.0mo (95% CI 8.4-12.4)
- π Disposition at 26.9mo: 38.5% still off-tx; 37.2% resumed ADT+ARPI per protocol; 9.0% started non-protocol tx
- π rPFS from interruption: 15/78 events, median NE (32.5-NE); 12-mo est 94.6% (89.6-99.9%)
- π OS: 4/78 events, median NE; causes: prostate cancer, MDS, influenza, MI
- β οΈ Single-arm; no randomized comparator vs continuous ADT+ARPI
- β οΈ 64.9% low-volume CHAARTED, 84.6% White; high-volume and diverse pts underrepresented
- Impact on long-term OS vs continuous ADT+ARPI: randomized trial needed
- Optimal re-initiation criteria in high-volume vs low-volume disease
- Biomarker predictors of durable treatment-free interval
π Sources Β· π¦ 1 tweet
Can treatment be safely stopped in selected patients with mHSPC?
— MJosΓ© Juan (@mjuanfi81) May 30, 2026
Phase II A-DREAM trial, 41% of responders remained treatment-free with testosterone recovery 18m after stopping ADT/ARPI. At a median FU of 21 months, 35% of patients required treatment re-initiation.@OncoAlert pic.twitter.com/iW2VDBWWhN
ENZAMET + Decipher Biomarker Analysis
FormHSPC, ADT + enzalutamide backbone, tumor tissue available for Decipher testing
TL;DRDecipher >0.85 identifies mHSPC pts with OS benefit from docetaxel intensification; IPTW interaction p=0.04, HR 0.75 (0.43-1.33).
- Framed as Level 1B evidence; consistent with CHARTED and STAMPEDE docetaxel predictive patterns
| Analysis | Decipher | Docetaxel HR (95% CI) | p | Interaction p |
|---|---|---|---|---|
| Unweighted | β€0.85 | 2.78 (1.49, 5.21) | 0.001 | 0.02 |
| Unweighted | >0.85 | 1.13 (0.71, 1.79) | 0.60 | β |
| IPTW | β€0.85 | 1.94 (0.95, 3.96) | 0.07 | 0.04 |
| IPTW | >0.85 | 0.75 (0.43, 1.33) | 0.33 | β |
+1 more figure
| Decipher | OS HR triplet vs doublet (95% CI) | p |
|---|---|---|
| β€0.85 | 3.02 (1.50-5.76) | β |
| >0.85 | 1.08 (0.60-1.71) | 0.73 |
4 details
- π Biomarker analysis within ENZAMET phase 3 RCT; ADT+enza+doce cohort N=320 with evaluable Decipher; DPMC 0.85 cutoff per statistical analysis plan
- β οΈ Individual arm HRs non-significant in IPTW-MVA (Decipher >0.85: HR 0.75, p=0.33; Decipher β€0.85: HR 1.94, p=0.07); signal rests on interaction term only
- β οΈ Tissue available in only ~427/3816 ENZAMET pts; representativeness of the analyzed subset uncertain
- β οΈ ENZAMET predated current ARSI-doublet SOC; Decipher model trained pre-ARPI β applicability to modern ADT+ARSI backbone unvalidated
- Prospective Decipher-guided triplet selection trial in ARPI-era mHSPC needed
- Optimal DPMC cutoff in pts receiving ADT+ARSI (not ENZA) doublets
π Sources Β· π¦ 2 tweets
#ASCO26 GU Oncology Spotlight π¨
— Dra. MarΓa Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
π¬ ENZAMET + Decipher | Part 2
Can genomics guide docetaxel intensification in mHSPC?
Outstanding presentation by @ChrisSweeney1.@OncoAlert@ASCO
After Part 1, the key question was:
β‘οΈ Can a genomic classifier identify which patients withβ¦ pic.twitter.com/nJYMxuXelV
#ASCO26 GU Oncology Spotlight π¨
— Dra. MarΓa Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
π¬ Precision Oncology: How to Apply New Biomarkers in Clinical Practice
Excellent discussion by Joshua M. Lang, MD, MS@JoshLangMD@OncoAlert@ASCO
This session captured the real challenge of precision oncology in GU cancers:
A biomarker is only⦠pic.twitter.com/ubfk49XPiM
ARACOG (AFT-47)
FormHSPC, nmCRPC, or mCRPC on ARSI; cognitive toxicity a concern
TL;DRMCCD median -36.1 (ENZ) vs -15.8 (DAR) at 24wk, p=0.009; enzalutamide caused significantly greater cognitive decline.
- Consistent with pharmacology: darolutamide has substantially lower CNS penetration vs enzalutamide, predicting less cognitive toxicity mechanistically
| Arm (N) | MCCD Module | Median Change |
|---|---|---|
| Darolutamide (48) | PALFAM | -15.8 |
| Enzalutamide (47) | SWM | -36.1 |
| P-value | 0.009 |
+1 more figure
6 details
- π Randomized open-label phase 2, N=111 (mHSPC, nmCRPC, mCRPC), DAR vs ENZ; enrolled 8/2021-3/2025
- π MCCD = maximally changed cognitive domain across 5 remote CANTAB tests: executive function, visual memory, attention, working memory
- π Darolutamide provided by study; enzalutamide through standard of care
- π 1Β° EP: CANTAB MCCD at 24wk median change -36.1 (ENZ, N=47) vs -15.8 (DAR, N=48), p=0.009
- β οΈ Open-label; crossover allowed before 24wk, analyzed at crossover timepoint in randomized arm
- β οΈ CANTAB modules are research instruments, not clinical cognitive diagnostic tools
- Cognitive difference durability beyond 24 weeks
- Whether MCCD effect size translates to clinically meaningful QoL impact
- Disease-state subgroup breakdown (mHSPC vs nmCRPC vs mCRPC)
π Sources Β· π¦ 2 tweets
#ASCO26 GU Oncology Spotlight π¨
— Dra. MarΓa Natalia Gandur Quiroga (@nataliagandur) May 30, 2026
π¬ Abstract 5005 | ARACOG / AFT-47
Cognitive effects of darolutamide vs enzalutamide
Presented by Alicia K. Morgans, MD, MPH, FASCO@CaPsurvivorship @OncoAlert@ASCO
In prostate cancer, we often discuss AR pathway inhibitors through the lens⦠pic.twitter.com/vpZr1w6kc6
ARACOG (AFT-47) met its primary endpoint: enzalutamide caused significantly greater cognitive decline than darolutamide at 24 weeks in advanced prostate cancer.
— Katy Beckermann (@katy_beckermann) May 30, 2026
Randomized open-label phase 2, 111 pts (mHSPC, mCRPC, nmCRPC), DAR vs ENZ.
Cognition was measured with CANTAB, a⦠pic.twitter.com/kj4vfGRVyp
TALAPRO-3
ForHRR-deficient metastatic hormone-sensitive prostate cancer
TL;DR3yr rPFS 77% vs 56% (HR 0.48, p<0.001) favoring talazoparib+enza+ADT in HRR-deficient mHSPC.
- vs TALAPRO-2 (talazoparib+enza, mCRPC, HRR+, HR ~0.46): class effect now established in hormone-sensitive setting
| Subgroup | n (exp/ctrl) | Median rPFS exp | Median rPFS ctrl | HR (95% CI) |
|---|---|---|---|---|
| ITT | 300/299 | NC (NC-NC) | 45.8 (37.7-NC) mo | 0.48 (0.36-0.65), p<0.001 |
| BRCA | 104/103 | NC (NC-NC) | 35.1 (18.6-NC) mo | 0.37 (0.22-0.61) |
| Non-BRCA | 196/196 | NC (NC-NC) | NC (40.5-NC) mo | 0.57 (0.39-0.82) |
3 details
- π Phase 3 RCT; N=599; HRR-deficient mHSPC; talazoparib+enza+ADT vs placebo+enza+ADT
CONSORT flow
- β οΈ Primary endpoint imaging-based rPFS, not OS; OS maturity not reported in source
- β οΈ Non-BRCA HRR effect attenuated (HR 0.57 vs BRCA HR 0.37); non-BRCA HRR subset heterogeneous
- OS benefit magnitude and maturity
- Which non-BRCA HRR alterations drive clinically meaningful rPFS benefit
- Post-progression sequencing in PARP-pretreated pts transitioning to mCRPC
π Sources Β· π¦ 1 tweet
JUST In: TALAPRO-3 published in @NEJM
— Toni Choueiri, MD (@DrChoueiri) May 30, 2026
Adding #talazoparib to enzalutamide/ADT
=>3-year rPFS: 77% vs 56% in HRR-deficient metastatic prostate cancer !
Looking forward to full presentation by @neerajaiims who keeps changing SOC, one trial at a time. @ASCO #ASCO26 @OncoAlert pic.twitter.com/nXiPk4DIXg
CHRYSALIS-2 (1L Ami+Laz, Atypical EGFR+)
ForAdvanced NSCLC, atypical EGFR mutation, treatment-naive
TL;DRMedian OS 41.0 mo (95% CI 27.7-NE) with ami+laz in 1L atypical EGFR+ advanced NSCLC; single-arm, n=49.
- Yang JCH NEJM 2025 (ami+laz 1L common EGFR): durable OS now reported in both common and atypical EGFR-mutated NSCLC populations
+1 more figure
7 details
- π Single-arm, n=49; 1L atypical EGFR-mutated advanced NSCLC
- π Median treatment duration 13.3 mo (range <0.1-53.2)
- π 39% remained on treatment >2 years
- π Median OS 41.0 mo (95% CI 27.7-NE); median follow-up 31.3 mo
- β οΈ Single-arm; no randomized comparator vs osimertinib or chemotherapy
- β οΈ Small N (49) limits any subgroup analysis by EGFR variant subtype
- β οΈ No clear EGFR variant subtype-outcome association found; underpowered to confirm or exclude
- Randomized trial vs osimertinib in atypical EGFR needed to confirm benefit
- CNS penetration and activity across atypical EGFR variant subtypes
- SC amivantamab formulation (COPERNICUS) applicability in this population
π Sources Β· π¦ 1 tweet
Amivantamab + lazertinib achieved a median OS of 41.0 months in treatment-naΓ―ve atypical EGFR-mutant NSCLC, with no clear association between EGFR variant subtype and outcome. A compelling option. Meanwhile, amivantamab continues evaluation across multiple tumor types. #ASCO26 pic.twitter.com/aWn3Ja60Ji
— Chul Kim (@chulkimMD) May 29, 2026
ESAONA
For1L EGFR-mutated NSCLC with active brain metastases
TL;DRIntracranial ORR 95.5% vs 79.6% (p=0.0004), iPFS HR 0.46 favoring asandeutertinib over osimertinib in 1L EGFR+ NSCLC with brain mets.
- Osimertinib established 1L SOC via FLAURA; ESAONA is first randomized head-to-head with a next-gen EGFR TKI in the brain-met-enriched setting
| Endpoint | Asandeutertinib | Osimertinib | HR / p |
|---|---|---|---|
| iORR (BICR) | 95.5% (89.8-98.5%) | 79.6% (71.0-86.6%) | p=0.0004 |
| Intracranial PFS | NR | 17.5 mo (15.18-NA) | HR 0.46, p=0.0020 |
| Overall PFS | NR | 17.2 mo (15.18-19.55) | HR 0.64, p=0.0473 |
5 details
- π Phase II, randomized, N=224; 1L EGFR-mutated NSCLC with brain mets, asandeutertinib (n=111) vs osimertinib (n=113)
- π Asandeutertinib: next-generation EGFR TKI evaluated head-to-head vs established osimertinib SOC
CONSORT flow
- β οΈ Safety (TRAEs)
- Any TRAEs: 99.1% (asandeutertinib) vs 95.6% (osimertinib)
- Serious TRAEs: 10.8% vs 7.1% β slightly higher in experimental arm
- β οΈ Phase 2 only, N=224; PFS medians not reached in experimental arm (immature); OS data not reported in source
- β οΈ Primary EP was iORR (response endpoint), not PFS or OS; longer follow-up required for survival readout
- Phase 3 OS confirmatory data needed before practice adoption
- Activity after progression on prior osimertinib unknown
- Optimal sequencing vs osimertinib + chemo (FLAURA2) in brain-met population
π Sources Β· π¦ 1 tweet
#ASCO26 π§ π
— Dr Rishabh Jain (@DrRishabhOnco) May 30, 2026
Could a next-generation EGFR TKI outperform osimertinib in patients with brain metastases?
The phase II ESAONA trial suggests the answer may be yes.
π§ͺ LBA2007 | ESAONA
1L EGFR-mutated NSCLC with brain metastases
π₯ n=224
βοΈ Asandeutertinib vs Osimertinib
Key⦠https://t.co/mEOKGNKgf7 pic.twitter.com/pUQuH6i2cV
OptiTROP-Lung05 NCT06448312
ForStage IIIB-IV NSCLC, PD-L1 TPS β₯1%, no EGFR/ALK, treatment-naive, ECOG 0-1
TL;DRmPFS NR vs 5.7mo, HR 0.35 (0.26-0.47), p<0.0001 favoring sac-TMT + pembro in 1L PD-L1+ NSCLC.
- Converges with TROPION-Lung08 (Dato-DXd+durvalumab vs pembro, TPSβ₯50%): ADC+IO > IO-mono signal emerging in 1L NSCLC
| Arm | Events n (%) | Median PFS (95%CI) | HR (95%CI) | p |
|---|---|---|---|---|
| Sac-TMT+Pembro (n=208) | 66 (31.7%) | NR (13.6, NE) | 0.35 (0.26, 0.47) | <0.0001 |
| Pembro (n=205) | 128 (62.4%) | 5.7mo (4.3, 7.0) | ref | β |
+3 more figures
| PD-L1 TPS | Sac-TMT+Pembro median PFS | Pembro median PFS | HR (95%CI) |
|---|---|---|---|
| β₯50% | NR (NE, NE) | 9.5mo (6.9, 13.8) | 0.47 (0.29, 0.77) |
| 1-49% | NR (11.1, NE) | 4.3mo (2.9, 5.5) | 0.28 (0.19, 0.41) |
8 details
- π Phase 3 open-label RCT; N=413; stage IIIB/IIIC/IV NSCLC; PD-L1 TPS β₯1%; no EGFR/ALK; ECOG 0-1
- π Sac-TMT 4mg/kg Q2W + pembro 400mg Q6W vs pembro 400mg Q6W; max 18 pembro cycles
CONSORT flow
- π 1Β° EP PFS by BICR: median NR (13.6, NE) vs 5.7mo (4.3, 7.0), HR 0.35 (95%CI 0.26-0.47), p<0.0001
- π ORR 70.2% vs 42.0%
- π Descriptive OS (immature): HR 0.55 (95%CI 0.36-0.85); events 33 (15.9%) vs 54 (26.3%); median f/u 10.5mo
- π PFS benefit consistent across both PD-L1 TPS subgroups (β₯50% and 1-49%)
- β οΈ OS immature at primary PFS analysis (10.5mo median f/u); definitive OS benefit not yet established
- β οΈ Control is pembro mono; for TPS 1-49%, pembro+platinum chemo is also SOC β no head-to-head vs chemo-IO doublet
- Will PFS benefit translate to OS with longer follow-up?
- Superiority vs. pembro + platinum chemo for TPS 1-49%?
- Predictive biomarker beyond PD-L1 TPS for TROP2 ADC benefit?
π Sources Β· π¦ 2 tweets
Right patient. Right treatment. Right timing.
— Yakup ErgΓΌn (@dr_yakupergun) May 30, 2026
The result: curves like theseπ#ASCO26 https://t.co/72KByLKz90
πREVIEW #ASCO26 #LCSM Oral
— Hidehito HORINOUCHI (@HHorinouchi) May 30, 2026
π₯OptiTROP-Lung05: 1L Sac-TMT + Pembro vs Pembro in PD-L1+ NSCLC
β mPFS NR vs 5.7m (HR 0.35)
β ORR 70.2% vs 42.0%
β OS HR 0.55 (95%CI 0.36-0.85, immature)
ποΈDr. Caicun Zhou
π https://t.co/DcbK1dGrhO@OncoAlert @Larvol @ASCO @IASLC https://t.co/512k6dZviW pic.twitter.com/Vdo86N50h9