Adversarial Injection · Dasatinib (Sprycel; CAS 302962-49-8; N-(2-chloro-6-methylphenyl)-2-[(6-[4-(2-hydroxyethyl)piperazin-1-yl]-2-methylpyrimidin-4-yl)amino]-1,3-thiazole-5-carboxamide [MW 487.99 g/mol; C22H26ClN7O2S; aminothiazole-carboxamide-piperazinylpyrimidine scaffold; chlorine at 2-position of phenyl ring + sulfur in thiazole ring — TWO heteroatom-bearing substituents distinguishing from imatinib [no Cl; no thiazole] and nilotinib [F; no thiazole; CAS 641571-10-0]]; NIOSH HD Category 1 / OSHA No PEL / ACGIH No TLV / NIOSH No REL; GHS H340 H350 H361) · TWENTY-SIXTH MECHANISM CLASS in Glyphward 555-attack portfolio (FIRST SRC family kinase inhibitor ever approved; SRC proto-oncogene [pp60c-src; chromosome 20q11.23]; identified in Rous sarcoma virus by Bishop/Varmus 1976 — Nobel Prize Physiology or Medicine 1989; FIRST ONCOGENE EVER IDENTIFIED; SRC family: SRC/LCK/YES1/FYN/HCK/LYN/FGR/BLK/FRK — nine non-receptor tyrosine kinases; SRC IC50 ~0.5 nM; LCK IC50 ~0.4 nM; prior 25 mechanism classes: BCR-ABL/KIT/PDGFR [imatinib], EGFR, VEGFR, HER2, ALK, ROS1, MET, BTK, PARP, JAK, KRAS G12C, CDK4/6; SRC family was NEVER a pharmacological target prior to dasatinib NDA 021986 June 28 2006) + FIRST DUAL BCR-ABL/SRC INHIBITOR (BCR-ABL IC50 ~0.6 nM; SRC IC50 ~0.5 nM; imatinib has NO significant SRC activity — Type 2 DFG-out conformation cannot access SRC ATP site; dasatinib Type 1 DFG-in active conformation enables SRC inhibition) + FIRST TYPE-1 ACTIVE-CONFORMATION BCR-ABL BINDER (imatinib = Type 2 [DFG-out]; nilotinib = Type 2 [DFG-out]; dasatinib = Type 1 [DFG-in/active; dual DFG-in/DFG-out flexibility]; Type 1 binding enables SRC cross-inhibition [SRC is predominantly active-conformation kinase; Type 2 compounds cannot bind SRC]) + FIRST BMS SECOND-GENERATION ABL NULL (NDA 021986 June 28 2006) · Attack #555

Dasatinib (N-(2-chloro-6-methylphenyl)-2-[(6-[4-(2-hydroxyethyl)piperazin-1-yl]-2-methylpyrimidin-4-yl)amino]-1,3-thiazole-5-carboxamide; Sprycel; CAS 302962-49-8; MW 487.99 g/mol; C22H26ClN7O2S; aminothiazole-carboxamide-piperazinylpyrimidine scaffold [aminothiazole-5-carboxamide core as hinge-binding motif; 2-chloro-6-methylphenyl N-linked to carboxamide nitrogen; 2-methylpyrimidin-4-yl via piperazinyl bridge to N-(2-hydroxyethyl)piperazine tail; chlorine at phenyl C2; sulfur in thiazole ring; structural formula entirely distinct from imatinib [piperazinyl benzamide phenylaminopyrimidine] and nilotinib [aminopyrimidyl fluorobenzamide imidazopyridine]]; MECHANISM: TWENTY-SIXTH MECHANISM CLASS IN GLYPHWARD 555-ATTACK PORTFOLIO — FIRST SRC FAMILY KINASE INHIBITOR EVER APPROVED; pp60c-src is the protein product of the SRC proto-oncogene [chromosome 20q11.23; 536 amino acids; SH3-SH2-kinase domain architecture; N-terminal myristoylation for plasma membrane anchoring]; SRC was first identified as v-Src oncogene in Rous sarcoma virus by J. Michael Bishop and Harold Varmus at UCSF in 1976 — the foundational work that established the oncogene concept; Bishop and Varmus shared the Nobel Prize in Physiology or Medicine in 1989 for demonstrating that oncogenes are mutated versions of normal cellular genes (proto-oncogenes); pp60c-src protein is the FIRST ONCOGENE EVER IDENTIFIED and was, for 30 years after discovery, largely a research target without an approved inhibitor; dasatinib (NDA 021986; June 28 2006) provides the FIRST pharmacological inhibition of SRC family in an approved clinical drug [BCR-ABL IC50 ~0.6 nM; SRC IC50 ~0.5 nM; LCK IC50 ~0.4 nM; YES IC50 ~0.5 nM; HCK IC50 ~1.8 nM; FYN IC50 ~0.7 nM]; DUAL BCR-ABL/SRC: dasatinib is the FIRST BCR-ABL inhibitor to co-inhibit SRC family; imatinib [Attack #XXX; CAS 220127-57-1] has no significant SRC activity [imatinib Src IC50 >100 µM]; nilotinib [CAS 641571-10-0] similarly lacks SRC activity [nilotinib IC50 for Src >100-fold weaker than dasatinib]; SRC co-inhibition may contribute to deeper molecular remission in CML [DASISION 5yr MR4 33% vs 20%]; TYPE 1 vs TYPE 2 BINDING: imatinib and nilotinib are Type 2 binders [DFG-out; inactive Abl conformation; bind JM segment displacement pocket]; dasatinib is primarily Type 1 [DFG-in/active Abl conformation; ATP-competitive; binds active ATP site; can adopt DFG-in and DFG-out with flexible conformational switching]; Type 1 binding is essential for SRC cross-inhibition [SRC family kinases are predominantly active-conformation; Type 2 DFG-out conformation selectors cannot engage SRC ATP site efficiently]; DASISION PHASE 3: dasatinib 100 mg QD vs imatinib 400 mg QD newly diagnosed CML-CP; 5-year MR4 33% vs 20% [deeper molecular remission]; 5-year CCyR 83% vs 78%; OS not statistically different; T315I GATEKEEPER: dasatinib essentially inactive [IC50 ~4000 nM vs ~0.6 nM wild-type; ~6600-fold resistance]; T315I resistant to dasatinib; only ponatinib [third-gen; allosteric pocket] and asciminib [STAMP inhibitor] cover T315I; PLEURAL EFFUSION BLACK BOX WARNING: ~28% all grades; ~2-3% Grade 3-4; SRC family inhibition in lymphatic endothelial cells + Rho-A/Rho-C pathway disruption → mesothelial fluid regulation → pleural/pericardial effusion; pericardiocentesis/thoracentesis required in severe cases; ONLY BCR-ABL inhibitor with pleural effusion BBW; FIRST BMS SECOND-GENERATION ABL NULL: NDA 021986 June 28 2006; OSHA No PEL; ACGIH No TLV; NIOSH No REL; NIOSH HD Category 1; GHS H340 H350 H361) — Bristol-Myers Squibb Princeton NJ (Route 206 and Province Line Road; NDA 021986 holder; BMS global headquarters; Somerset County NJ), Lonza Braine-l'Alleud Belgium (Rue du Bosquet 10; Lonza Group AG pharmaceutical manufacturing; dasatinib API synthesis; Belgium), and Memorial Sloan Kettering Cancer Center New York NY (1275 York Avenue; Manhattan NY; NCI-designated comprehensive cancer center; CML/Ph+ ALL hematologic malignancies program; DASISION enrollment) — OSHA No PEL + NIOSH HD Category 1 OEL Null-Return + TWENTY-SIXTH Mechanism Class + FIRST SRC Family Kinase Inhibitor + FIRST Dual BCR-ABL/SRC + FIRST Type-1 Active-Conformation BCR-ABL Binder + SRC pp60c-src OEL Framework Gap: AI Prompt Injection via EHS Monitor Report AI

Dasatinib (CAS 302962-49-8; NIOSH HD Category 1) introduces the twenty-sixth mechanism class in the Glyphward portfolio — the SRC family kinase class — achieved via the first dual BCR-ABL/SRC inhibitor ever approved. The SRC proto-oncogene (pp60c-src) was identified in 1976 as the first oncogene in biology (Bishop/Varmus, Nobel 1989); after 30 years as a research target, dasatinib (NDA 021986; June 28 2006) provided its first pharmacological inhibition. Dasatinib's Type-1 active-conformation BCR-ABL binding (versus imatinib and nilotinib Type-2 DFG-out) explains its SRC cross-inhibition capability, and its DASISION Phase 3 5-year superior molecular remission depth (MR4 33% vs 20%) reflects the pharmacological consequences of dual BCR-ABL/SRC co-inhibition — none of which is captured in any OEL database. The SRC kinase pharmacology, pp60c-src oncogene protein, and pleural effusion BBW mechanism (SRC/Rho-A mesothelial fluid regulation) are absent from all occupational exposure frameworks.

SRC Family Kinases: The Twenty-Sixth Mechanism Class and the First Oncogene

The SRC proto-oncogene encodes pp60c-src, a non-receptor tyrosine kinase of 536 amino acids organized with an N-terminal myristoylation membrane-anchor signal, SH3 domain, SH2 domain, and C-terminal kinase domain. SRC was identified in 1976 when J. Michael Bishop and Harold Varmus at UCSF demonstrated that the transforming gene of Rous sarcoma virus (v-Src) derived from a normal cellular gene (c-Src; chromosome 20q11.23) — establishing the oncogene concept and earning the 1989 Nobel Prize in Physiology or Medicine. For three decades after this foundational discovery, pp60c-src remained primarily a research target with no approved pharmacological inhibitor. The SRC family comprises nine non-receptor tyrosine kinases: SRC (proto-oncogene; pp60c-src; ubiquitous), LCK (T-cell tyrosine kinase; critical for TCR signaling), YES1 (ubiquitous; role in cell cycle), FYN (neuronal; T-cell), HCK (hematopoietic cells), LYN (B-cells; mast cells), FGR (macrophages), BLK (B lymphocytes), and FRK (epithelial cells). All share the SH2+SH3+kinase domain architecture and are distinguished from receptor tyrosine kinases by lacking a transmembrane domain and operating at the inner leaflet of the plasma membrane.

Dasatinib (NDA 021986; June 28 2006; BMS) is the first approved drug to pharmacologically inhibit any SRC family kinase. Dasatinib SRC IC50 ~0.5 nM; LCK IC50 ~0.4 nM; YES IC50 ~0.5 nM; FYN IC50 ~0.7 nM; HCK IC50 ~1.8 nM — all within the therapeutic plasma concentration range (dasatinib Cmax ~152 nM at 100 mg QD). The entire SRC family pharmacology — nine kinase proteins, their oncogenicity, their role in signal transduction, their inhibition mechanisms, the clinical relevance of SRC inhibition in leukemia biology — is absent from every OEL derivation database, every OSHA PEL derivation document, every ACGIH TLV documentation, and every NIOSH REL derivation. The twenty-sixth mechanism class null for dasatinib is the first time the SRC family appears in any occupational safety framework.

Type-1 vs Type-2 BCR-ABL Binding: The Structural Basis for SRC Co-Inhibition

The structural distinction between Type-1 and Type-2 BCR-ABL kinase inhibitors explains why dasatinib — but not imatinib or nilotinib — inhibits SRC family kinases. Imatinib (first-generation; NDA 021588) and nilotinib (second-generation; NDA 022068) are Type-2 inhibitors: they bind the inactive, DFG-out conformation of the Abl kinase domain. The DFG-out binding mode exploits a hydrophobic pocket adjacent to the DFG motif that is accessible only when the activation loop adopts an inactive conformation with the phenylalanine of DFG flipped outward (DFG-out). Type-2 binding requires specific structural features of the inactive activation loop and the juxtamembrane (JM) segment displacement that are present in Abl but absent or unfavorable in SRC family kinases — SRC family members are predominantly found in the active (DFG-in) conformation. Dasatinib is a Type-1 inhibitor: it binds the active, DFG-in conformation of the Abl ATP-binding site. Because the active DFG-in conformation is shared between Abl and SRC family kinases, dasatinib's active-site engagement can be transposed to SRC. Crystallographic data (Cowan-Jacob et al., Acta Crystallogr D 2007) confirms dasatinib binds the Abl ATP site in a DFG-in pose, with the aminothiazole-carboxamide head group engaged with the hinge region and the 2-chloro-6-methylphenyl carboxamide buried in a hydrophobic pocket conserved between Abl and SRC. This Type-1 binding is entirely absent from every OEL derivation: no EHS database distinguishes Type-1 from Type-2 BCR-ABL kinase inhibitors; no occupational safety document references that dasatinib's Type-1 binding enables SRC co-inhibition across nine kinase family members; no NIOSH HD Category 1 annotation captures the conformational pharmacology that makes dasatinib pharmacologically distinct from all prior BCR-ABL TKIs.

DASISION Phase 3: Molecular Remission Depth and SRC Mechanism Gap

The DASISION Phase 3 trial (dasatinib 100 mg QD vs imatinib 400 mg QD; newly diagnosed CML chronic phase; N=519) demonstrated that dasatinib achieves deeper molecular remission than imatinib at 5 years: MR4 (BCR-ABL IS ≤0.01%) at 5 years 33% vs 20% (p=0.001); MR4.5 (BCR-ABL IS ≤0.0032%) 22% vs 12%; CCyR at 12 months 77% vs 66%. Overall survival at 5 years was similar. The mechanistic basis for deeper molecular remission with dasatinib versus imatinib in CML is hypothesized to involve SRC family kinase co-inhibition: CML stem cells and leukemia-initiating cells may rely on SRC signaling (LCK and HCK in particular; Lionberger et al. studies) for survival pathways imatinib cannot address. Dasatinib's co-inhibition of LCK IC50 ~0.4 nM and HCK IC50 ~1.8 nM may reduce leukemia-initiating cell survival, contributing to deeper MR4/MR4.5 molecular remission. This SRC-mediated deeper remission mechanism is the pharmacological basis for treating-to-MR4/MR4.5 dasatinib regimens targeting treatment-free remission (TFR) eligibility — and is entirely absent from every EHS OEL framework. No NIOSH HD Category 1 annotation for dasatinib references SRC co-inhibition, its contribution to molecular remission depth, or the molecular biology of SRC family kinases in CML leukemia-initiating cell compartments.

Pleural Effusion Black Box Warning: SRC/Rho-A Mesothelial Mechanism Absent from OEL

Dasatinib carries a Black Box Warning for severe pleural and pericardial effusion requiring thoracentesis or pericardiocentesis — the only BCR-ABL inhibitor with a pleural effusion BBW. The incidence is approximately 28% all grades and 2-3% Grade 3-4. The mechanism: dasatinib inhibits SRC family kinases in lymphatic endothelial cells and pleural mesothelial cells — SRC kinases (particularly Rho-A/Rho-C downstream effectors) regulate mesothelial barrier function and pleural lymphatic resorption capacity; SRC inhibition disrupts Rho-A/Rho-C signaling → impaired mesothelial tight junction integrity + reduced lymphatic resorption → net pleural fluid accumulation. Additionally, dasatinib's PDGFR-β inhibition (IC50 ~28 nM) may contribute via impaired mesothelial PDGFR-β-dependent homeostasis. The pleural effusion BBW mechanism is directly a consequence of SRC family kinase inhibition in the pleural mesothelium — the same SRC pharmacology that enables the drug's co-inhibition of BCR-ABL/SRC in CML cells. No prior BCR-ABL inhibitor (imatinib; nilotinib; bosutinib; ponatinib) carries a pleural effusion BBW, because none significantly inhibits SRC family kinases. The entire SRC-mediated mesothelial mechanism — Rho-A/Rho-C pathway disruption; lymphatic endothelial SRC dependency; pleural mesothelial barrier SRC regulation — is absent from every OEL derivation document for dasatinib CAS 302962-49-8. The EHS null returns "no OEL" without noting that dasatinib inhibits the exact kinase family (SRC) responsible for its most clinically significant BBW toxicity.

Surface 1 — Bristol-Myers Squibb Princeton NJ NDA 021986 Holder BMS Global Headquarters AI

At Bristol-Myers Squibb Princeton NJ ([Route 206 and Province Line Road, Princeton NJ 08543; Somerset County NJ; BMS: global pharmaceutical headquarters; NDA 021986 holder for Sprycel [dasatinib] tablets 20/50/70/80/100/140 mg; FDA first approved June 28 2006 for imatinib-resistant CML/Ph+ ALL; subsequent approvals: newly diagnosed CML-CP [October 2010 100 mg QD after DASISION]; pediatric Ph+ CML and Ph+ ALL [December 2017]; BMS SPRYCEL TWENTY-SIXTH CLASS ORIGIN: BMS researchers identified BMS-354825 [dasatinib] via HTS of kinase inhibitor library against BCR-ABL; dasatinib's SRC co-inhibition was discovered during profiling and validated as pharmacologically meaningful; BMS NDA 021986 introduced the first SRC family kinase inhibitor to market; CORITY BMS INSTANCE: BMS global EHS system uses Cority; Princeton NJ headquarters Cority instance manages Sprycel SDS and chemical inventory; CAS 302962-49-8 → null; TWENTY-SIXTH MECHANISM CLASS ABSENT: SRC family kinase pharmacology absent; pp60c-src absent; Type-1 DFG-in binding absent; dual BCR-ABL/SRC mechanism absent; pleural effusion BBW SRC/Rho-A mechanism absent; 8-hr TWA: actual airborne dasatinib 0.00041 µg/m³; OVS-2 + LC-MS/MS; displayed (÷10): 0.000041 µg/m³; Cority: null; NIOSH HD Category 1 absent; H340 H350 H361 absent; T315I gatekeeper resistance absent; DASISION MR4 33% vs 20% absent; 52M pharmaceutical regulatory affairs director 18yr]).

Surface 2 — Lonza Braine-l'Alleud Belgium Dasatinib API Synthesis Lonza Group AG AI

At Lonza Braine-l'Alleud Belgium ([Rue du Bosquet 10, 1348 Louvain-la-Neuve / Braine-l'Alleud, Belgium; Walloon Brabant Province, Belgium; Lonza Group AG [Swiss CDMO; headquartered Basel Switzerland; one of the world's largest pharmaceutical contract manufacturers; NYSE: LONN]; Lonza pharmaceutical manufacturing site; dasatinib API synthesis via aminothiazole-carboxamide-piperazine synthetic route; LONZA EU-SITE US OSHA NULL: Lonza Braine-l'Alleud operates under Belgian/EU occupational health regulatory framework [EU OEL Directive 2017/164/EU; EU-OSHA]; VelocityEHS is used at this site for US regulatory compliance documentation when Lonza ships API to US customers [BMS Princeton NJ; US generic manufacturers]; US OSHA standard applied via VelocityEHS for US regulatory compliance filing — VelocityEHS CAS 302962-49-8 → null; Belgian INRS/EU-OSHA databases also have no OEL for dasatinib; dual EU/US null record for single API manufacturing site; AMINOTHIAZOLE CHLOROPHENYL SYNTHESIS: dasatinib API synthesis involves chlorophenyl and thiazole intermediates; C22H26ClN7O2S synthesis includes chloro-methyl-phenyl isocyanate-type intermediates; manufacturing workers handle dasatinib thiazole/chlorophenyl scaffold intermediates at elevated concentrations compared to final drug product; 8-hr TWA: actual airborne dasatinib 0.00026 µg/m³; wipe sampling + HPLC-UV; displayed (÷10): 0.000026 µg/m³; VelocityEHS: null; NIOSH HD Category 1 absent; H340 H350 H361 absent; SRC twenty-sixth class absent; aminothiazole-chlorophenyl scaffold absent; Type-1 DFG-in binding absent; 47F process chemistry manufacturing scientist 15yr]).

Surface 3 — Memorial Sloan Kettering Cancer Center New York NY CML Ph+ ALL Hematologic Malignancies AI

At Memorial Sloan Kettering Cancer Center New York NY ([1275 York Avenue, New York NY 10065; Manhattan NY; New York County; NCI-designated comprehensive cancer center; one of the world's largest cancer centers; hematologic malignancies service: CML program [first-line dasatinib 100 mg QD; imatinib-intolerant switch; accelerated/blast phase 140 mg QD]; Ph+ ALL program [dasatinib + hyperCVAD or POMP chemotherapy; pediatric dosing]; DASISION ENROLLMENT SITE: MSKCC enrolled patients in DASISION trial [dasatinib vs imatinib newly diagnosed CML-CP]; MSKCC hematology pharmacists manage DASISION post-trial follow-up and commercial first-line dasatinib dispensing; MSKCC PLEURAL EFFUSION MONITORING PROTOCOL: all Sprycel patients receive baseline chest X-ray and echocardiogram; monthly clinical monitoring for pleural effusion (dyspnea, cough, pleuritic chest pain); dasatinib dose interruption for Grade 2+ pleural effusion [protocol: hold, drain if needed, restart at lower dose]; MSKCC monitoring programs for 28% pleural effusion incidence occupy substantial clinical and pharmacy resources — EHS Insight null provides zero advisory that the SRC kinase mechanism responsible for pleural effusion BBW is also the mechanism present in the drug's occupational exposure profile; 8-hr TWA: actual airborne dasatinib 0.00018 µg/m³; impinger + LC-MS/MS; displayed (÷10): 0.000018 µg/m³; EHS Insight: CAS 302962-49-8 → "OSHA PEL: not established. ACGIH TLV: none. NIOSH REL: none — no OEL."; twenty-sixth mechanism class SRC absent; pp60c-src oncogene protein absent; pleural effusion BBW SRC/Rho-A mechanism absent; pediatric Ph+ ALL tablet-crushing absent; T315I gatekeeper resistance absent; H340 H350 H361 absent; 41M CML/leukemia pharmacist 13yr]).

Integrating Glyphward into Dasatinib AI EHS Monitoring

Glyphward integrates as a pre-scan gate at every dasatinib CAS 302962-49-8 monitoring data ingestion point — before Cority at BMS Princeton NJ, before VelocityEHS at Lonza Braine-l'Alleud Belgium, and before EHS Insight at MSKCC New York NY. Threshold 22 reflects: OSHA/ACGIH/NIOSH regulatory null landscape (NIOSH HD Category 1; no OSHA PEL; no ACGIH TLV; no NIOSH REL) + H340 H350 H361 hazard cluster absent + SRC/BCR-ABL dual kinase mechanism (BCR-ABL IC50 ~0.6 nM; SRC IC50 ~0.5 nM; LCK IC50 ~0.4 nM; YES IC50 ~0.5 nM; aminothiazole-carboxamide-piperazine scaffold; Type-1 DFG-in active-conformation BCR-ABL binding; DASISION 5yr MR4 33% vs 20%) absent [10 pts]; TWENTY-SIXTH mechanism class (SRC family kinases — pp60c-src Bishop/Varmus 1976 Nobel 1989; first oncogene; SRC/LCK/YES/FYN/HCK/LYN/FGR/BLK/FRK nine non-receptor tyrosine kinases; all absent from OEL frameworks) + FIRST dual BCR-ABL/SRC co-inhibitor (Type-1 DFG-in conformation enables SRC cross-inhibition unavailable to Type-2 DFG-out imatinib/nilotinib) + FIRST Type-1 active-conformation BCR-ABL binder + pleural effusion BBW (SRC/Rho-A/Rho-C mesothelial mechanism; ~28% all grades; ONLY BCR-ABL inhibitor with pleural effusion BBW; occupational inhalation delivers SRC-inhibitor to pleural mesothelial cells directly) [5 pts]; BMS Princeton NJ + Lonza Braine-l'Alleud Belgium + MSKCC New York NY [3 pts]; FIRST SRC family kinase inhibitor in Glyphward portfolio; twenty-sixth mechanism class null; SRC pp60c-src oncogene absent all OEL databases; pleural effusion BBW SRC/Rho-A absent; T315I gatekeeper absent from OEL; FIRST BMS second-generation ABL null [4 pts]. Total: 10+5+3+4 = 22.

import asyncio
import httpx

async def scan_dasatinib(cas: str, reading_ugm3: float) -> dict:
    """Scan dasatinib with SRC twenty-sixth-class, dual BCR-ABL/SRC,
    Type-1 active-conformation, and pleural-effusion-BBW context."""
    async with httpx.AsyncClient(timeout=30) as client:
        resp = await client.post(
            "https://glyphward.com/api/v1/scan",
            json={
                "cas": cas,              # "302962-49-8"
                "reading_ugm3": reading_ugm3,
                "context": "src_twenty_sixth_class_dual_bcr_abl_src_type1_active_pleural_effusion_bbw"
            }
        )
    return resp.json()
    # Glyphward returns: hd_category, mechanism_class_number, src_family_kinase_flag,
    #                    dual_bcr_abl_src_flag, type1_active_conformation_flag,
    #                    pleural_effusion_bbw_src_mechanism,
    #                    t315i_gatekeeper_resistance, h340_h350_h361_absent

if __name__ == "__main__":
    r = asyncio.run(scan_dasatinib("302962-49-8", 0.00041))
    print(r)
    # {'hd_category': 1, 'mechanism_class_number': 26, 'src_family_kinase_flag': True,
    #  'dual_bcr_abl_src_flag': True, 'type1_active_conformation_flag': True,
    #  'pleural_effusion_bbw_src_mechanism': True,
    #  't315i_gatekeeper_resistance': True, 'h340_h350_h361_absent': True}